1. Exercise and Coronary Atherosclerosis: Observations, Explanations, Relevance, and Clinical Management.
作者:Aengevaeren Vincent L , Mosterd Arend , Sharma Sanjay , Prakken Niek H J , Möhlenkamp Stefan , Thompson Paul D , Velthuis Birgitta K , Eijsvogels Thijs M H
期刊:Circulation
日期:2020-04-20
DOI :10.1161/CIRCULATIONAHA.119.044467
Physical activity and exercise training are effective strategies for reducing the risk of cardiovascular events, but multiple studies have reported an increased prevalence of coronary atherosclerosis, usually measured as coronary artery calcification, among athletes who are middle-aged and older. Our review of the medical literature demonstrates that the prevalence of coronary artery calcification and atherosclerotic plaques, which are strong predictors for future cardiovascular morbidity and mortality, was higher in athletes compared with controls, and was higher in the most active athletes compared with less active athletes. However, analysis of plaque morphology revealed fewer mixed plaques and more often only calcified plaques among athletes, suggesting a more benign composition of atherosclerotic plaques. This review describes the effects of physical activity and exercise training on coronary atherosclerosis in athletes who are middle-aged and older and aims to contribute to the understanding of the potential adverse effects of the highest doses of exercise training on the coronary arteries. For this purpose, we will review the association between exercise and coronary atherosclerosis measured using computed tomography, discuss the potential underlying mechanisms for exercise-induced coronary atherosclerosis, determine the clinical relevance of coronary atherosclerosis in middle-aged athletes and describe strategies for the clinical management of athletes with coronary atherosclerosis to guide physicians in clinical decision making and treatment of athletes with elevated coronary artery calcification scores.
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1区Q1影响因子: 8
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2. Innate immune cells in the pathophysiology of calcific aortic valve disease: lessons to be learned from atherosclerotic cardiovascular disease?
期刊:Basic research in cardiology
日期:2022-05-17
DOI :10.1007/s00395-022-00935-6
Calcific aortic valve disease (CAVD) is the most common valvular disease in the developed world with currently no effective pharmacological treatment available. CAVD results from a complex, multifactorial process, in which valvular inflammation and fibro-calcific remodelling lead to valve thickening and cardiac outflow obstruction. The exact underlying pathophysiology of CAVD is still not fully understood, yet the development of CAVD shows many similarities with the pathophysiology of atherosclerotic cardiovascular disease (ASCVD), such as coronary artery disease. Innate immune cells play a crucial role in ASCVD and might also play a pivotal role in the development of CAVD. This review summarizes the current knowledge on the role of innate immune cells, both in the circulation and in the aortic valve, in the development of CAVD and the similarities and differences with ASCVD. Trained immunity and clonal haematopoiesis of indeterminate potential are proposed as novel immunological mechanisms that possibly contribute to the pathophysiology of CAVD and new possible treatment targets are discussed.
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3区Q1影响因子: 4.9
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3. Senescent Microvesicles: A Novel Advance in Molecular Mechanisms of Atherosclerotic Calcification.
期刊:International journal of molecular sciences
日期:2018-07-09
DOI :10.3390/ijms19072003
Atherosclerosis, a chronic inflammatory disease that causes the most heart attacks and strokes in humans, is the leading cause of death in the developing world; its principal clinical manifestation is coronary artery disease. The development of atherosclerosis is attributed to the aging process itself (biological aging) and is also associated with the development of chronic diseases (premature aging). Both aging processes produce an increase in risk factors such as oxidative stress, endothelial dysfunction and proinflammatory cytokines (oxi-inflamm-aging) that might generate endothelial senescence associated with damage in the vascular system. Cellular senescence increases microvesicle release as carriers of molecular information, which contributes to the development and calcification of atherosclerotic plaque, as a final step in advanced atherosclerotic plaque formation. Consequently, this review aims to summarize the information gleaned to date from studies investigating how the senescent extracellular vesicles, by delivering biological signalling, contribute to atherosclerotic calcification.
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4区Q2影响因子: 1.3
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4. Nonalcoholic Fatty Liver Disease: An Emerging Modern-Day Risk Factor for Cardiovascular Disease.
期刊:Cureus
日期:2022-05-30
DOI :10.7759/cureus.25495
Nonalcoholic fatty liver disease (NAFLD), also named metabolic dysfunction-associated fatty liver disease (MAFLD), is a progressive disease spectrum encompassing simple steatosis, nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. It is a clinically silent disease leading to multiple extra-hepatic complications/comorbidities. It is an independent risk factor for cardiovascular disease (CVD), increasing susceptibility to hypertension, atherosclerosis, arrhythmia, myocardial dysfunction, cardiac valve deformation, and venous thrombosis through putative mechanisms including systemic inflammation, endothelial dysfunction, oxidative stress, insulin resistance, and altered lipid metabolism. Eventually, it increases the CVD prevalence, incident, and fatality, contributing to a huge health care burden. In fact, CVD is becoming the leading cause of mortality among patients with NAFLD. Other cardiometabolic risk factors coexisting with NAFLD may also accelerate the synergistic development of CVD, which warrants assessment targeting hypertension, diabetes mellitus (DM), obesity, and dyslipidemia to be an integral part of NAFLD care. Monitoring metabolic biomarkers (glucose, glycosylated hemoglobin [HbA1c], insulin, lipids, and lipoproteins), cardiovascular (CV) risk scores (American College of Cardiology/American Heart Association [ACC/AHA] or Framingham), and subclinical atherosclerosis (coronary artery calcification [CAC], carotid intima-media thickness [CIMT], and carotid plaque) are recommended for risk prediction and reduction. There is no universally accepted treatment for NAFLD, and lifestyle changes with weight loss of at least 10% are the mainstay of management. Combination therapy of ezetimibe and statins have a cardioprotective effect and help reduce liver fat. Despite being an emerging risk factor for CVD and its rapidly increasing pattern affecting a quarter of the global population, NAFLD remains overlooked and undetected, unlike the other traditional risk factors. Hence, we conducted a comprehensive narrative review to shed more light on the importance of screening CVD in NAFLD patients. PubMed indexed relevant articles published from 2002 to 2022 (20 years) were searched in April 2022 using medical subject headings (MeSH) as "nonalcoholic fatty liver disease" [Mesh] AND "cardiovascular diseases" [Mesh]. Evidence from 40 observational studies, three clinical trials, one case series, 45 narrative reviews, four systematic reviews and meta-analyses, three systematic reviews, and one meta-analysis were summarized on the epidemiologic data, pathophysiologic mechanisms, clinical features, diagnostic modalities, overlapping management, perceived challenges and health literacy regarding the CVD risk attributed to NAFLD.
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2区Q1影响因子: 5.1
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5. Changes of the coronary arteries and cardiac microvasculature with aging: Implications for translational research and clinical practice.
作者:Piccirillo Francesco , Carpenito Myriam , Verolino Giuseppe , Chello Camilla , Nusca Annunziata , Lusini Mario , Spadaccio Cristiano , Nappi Francesco , Di Sciascio Germano , Nenna Antonio
期刊:Mechanisms of ageing and development
日期:2019-10-21
DOI :10.1016/j.mad.2019.111161
Aging results in functional and structural changes in the cardiovascular system, translating into a progressive increase of mechanical vessel stiffness, due to a combination of changes in micro-RNA expression patterns, autophagy, arterial calcification, smooth muscle cell migration and proliferation. The two pivotal mechanisms of aging-related endothelial dysfunction are oxidative stress and inflammation, even in the absence of clinical disease. A comprehensive understanding of the aging process is emerging as a primary concern in literature, as vascular aging has recently become a target for prevention and treatment of cardiovascular disease. Change of life-style, diet, antioxidant regimens, anti-inflammatory treatments, senolytic drugs counteract the pro-aging pathways or target senescent cells modulating their detrimental effects. Such therapies aim to reduce the ineluctable burden of age and contrast aging-associated cardiovascular dysfunction. This narrative review intends to summarize the macrovascular and microvascular changes related with aging, as a better understanding of the pathways leading to arterial aging may contribute to design new mechanism-based therapeutic approaches to attenuate the features of vascular senescence and its clinical impact on the cardiovascular system.
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4区Q2影响因子: 1.6
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6. Association of bone mineral density and trabecular bone score with cardiovascular disease.
期刊:Tzu chi medical journal
日期:2020-01-17
DOI :10.4103/tcmj.tcmj_234_19
Traditionally, osteoporosis and cardiovascular disease (CVD) are considered as separate chronic diseases. Increasing evidence now links osteoporosis with hypertension, abnormal lipid metabolism, atherosclerosis, vascular calcification (VC), and congestive heart failure. VC coexists with bone loss, and aortic calcification is a strong predictor of low bone mineral density (BMD) and fragility fractures. The same holds true for coronary artery calcification (CAC): the lower the BMD, the higher the CAC. Trabecular bone score (TBS) iNsight software can analyze the existing BMD database to obtain the bony microstructure score (TBS). Many TBS-related studies include fracture risk, normal aging, diabetes, potential genes, obesity, and asthma severity prediction. The inverse relationship of TBS to VC may provide insight into bone-vascular interactions in chronic kidney disease. A higher TBS has been associated with moderate, but not high, CAC. One explanation is that bone microstructural remodeling becomes more active during early coronary calcification. Increased risk of 10-year likelihood of hip fracture and major osteoporotic fracture as estimated by the fracture risk assessment tool FRAX is significantly and independently associated with more severe CAC scores. Dual-energy X-ray absorptiometry and FRAX can be used to predict fracture risk and CAC scores, identifying patients who may benefit from early intervention. This review will discuss the relationship and possible mechanism of BMD, TBS, and FRAX with CVD and VC or CAC.
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3区Q1影响因子: 4.2
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7. Emerging Evidence Linking the Liver to the Cardiovascular System: Liver-derived Secretory Factors.
期刊:Journal of clinical and translational hepatology
日期:2023-05-12
DOI :10.14218/JCTH.2022.00122
Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide. Recently, accumulating evidence has revealed hepatic mediators, termed as liver-derived secretory factors (LDSFs), play an important role in regulating CVDs such as atherosclerosis, coronary artery disease, thrombosis, myocardial infarction, heart failure, metabolic cardiomyopathy, arterial hypertension, and pulmonary hypertension. LDSFs presented here consisted of microbial metabolite, extracellular vesicles, proteins, and microRNA, they are primarily or exclusively synthesized and released by the liver, and have been shown to exert pleiotropic actions on cardiovascular system. LDSFs mainly target vascular endothelial cell, vascular smooth muscle cells, cardiomyocytes, fibroblasts, macrophages and platelets, and further modulate endothelial nitric oxide synthase/nitric oxide, endothelial function, energy metabolism, inflammation, oxidative stress, and dystrophic calcification. Although some LDSFs are known to be detrimental/beneficial, controversial findings were also reported for many. Therefore, more studies are required to further explore the causal relationships between LDSFs and CVDs and uncover the exact mechanisms, which is expected to extend our understanding of the crosstalk between the liver and cardiovascular system and identify potential therapeutic targets. Furthermore, in the case of patients with liver disease, awareness should be given to the implications of these abnormalities in the cardiovascular system. These studies also underline the importance of early recognition and intervention of liver abnormalities in the practice of cardiovascular care, and a multidisciplinary approach combining hepatologists and cardiologists would be more preferable for such patients.
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3区Q1影响因子: 2.6
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8. Cardiovascular risk factors in children on dialysis: an update.
作者:Querfeld Uwe , Schaefer Franz
期刊:Pediatric nephrology (Berlin, Germany)
日期:2018-10-31
DOI :10.1007/s00467-018-4125-x
Cardiovascular disease (CVD) is a life-limiting comorbidity in patients with chronic kidney disease (CKD). In childhood, imaging studies have demonstrated early phenotypic characteristics including increases in left ventricular mass, carotid artery intima-media thickness, and pulse wave velocity, which occur even in young children with early stages of CKD. Vascular calcifications are the signature of an advanced phenotype and are mainly found in adolescents and young adults treated with dialysis. Association studies have provided valuable information regarding the significance of a multitude of risk factors in promoting CVD in children with CKD by using intermediate endpoints of measurements of surrogate parameters of CVD. Dialysis aggravates pre-existing risk factors and accelerates the progression of CVD with additional dialysis-related risk factors. Coronary artery calcifications in children and young adults with CKD accumulate in a time-dependent manner on dialysis. Identification of risk factors has led to improved understanding of principal mechanisms of CKD-induced damage to the cardiovascular system. Treatment strategies include assessment and monitoring of individual risk factor load, optimization of treatment of modifiable risk factors, and intensified hemodialysis if early transplantation is not possible.
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1区Q1影响因子: 9.2
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9. Arterial ageing: from endothelial dysfunction to vascular calcification.
期刊:Journal of internal medicine
日期:2017-03-27
DOI :10.1111/joim.12605
Complex structural and functional changes occur in the arterial system with advancing age. The aged artery is characterized by changes in microRNA expression patterns, autophagy, smooth muscle cell migration and proliferation, and arterial calcification with progressively increased mechanical vessel rigidity and stiffness. With age the vascular smooth muscle cells modify their phenotype from contractile to 'synthetic' determining the development of intimal thickening as early as the second decade of life as an adaptive response to forces acting on the arterial wall. The increased permeability observed in intimal thickening could represent the substrate on which low-level atherosclerotic stimuli can promote the development of advanced atherosclerotic lesions. In elderly patients the atherosclerotic plaques tend to be larger with increased vascular stenosis. In these plaques there is a progressive accumulation of both lipids and collagen and a decrease of inflammation. Similarly the plaques from elderly patients show more calcification as compared with those from younger patients. The coronary artery calcium score is a well-established marker of adverse cardiovascular outcomes. The presence of diffuse calcification in a severely stenotic segment probably induces changes in mechanical properties and shear stress of the arterial wall favouring the rupture of a vulnerable lesion in a less stenotic adjacent segment. Oxidative stress and inflammation appear to be the two primary pathological mechanisms of ageing-related endothelial dysfunction even in the absence of clinical disease. Arterial ageing is no longer considered an inexorable process. Only a better understanding of the link between ageing and vascular dysfunction can lead to significant advances in both preventative and therapeutic treatments with the aim that in the future vascular ageing may be halted or even reversed.
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3区Q2影响因子: 2.1
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10. Effects of fetuin-A with diverse functions and multiple mechanisms on human health.
作者:Icer Mehmet Arif , Yıldıran Hilal
期刊:Clinical biochemistry
日期:2020-11-25
DOI :10.1016/j.clinbiochem.2020.11.004
Fetuin-A (Alfa 2-Heremans-Schmid) is a glycoprotein that is mainly synthesized by hepatocytes and then released into the bloodstream. While fetuin-A, a multifunctional protein, has inhibitory effects on health in the processes of calcification, mineralization, coronary artery calcification (CAC), and kidney stone formation by various mechanisms, it has such stimulatory effects as obesity, diabetes, and tumor progression processes. Fetuin-A produces these effects on the organism mainly by playing a role in the secretion levels of some inflammatory cytokines and exosomes, preventing unwanted calcification, inhibiting the autophosphorylation of tyrosine kinase, suppressing the release of adiponectin and peroxisome proliferator-activated receptor-γ (PPARγ), activating the toll-like receptor 4 (TLR-4), triggering the phosphatidylinositol 3 (PI3) kinase/Akt signaling pathway and cell proliferation, and mimicking the transforming growth factor-beta (TGF-β) receptor. In the present review, fetuin-A was examined in a wide perspective from the structure and release of fetuin-A to its effects on health.
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3区Q1影响因子: 4
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11. Molecular and Cellular Mechanisms that Induce Arterial Calcification by Indoxyl Sulfate and P-Cresyl Sulfate.
作者:Opdebeeck Britt , D'Haese Patrick C , Verhulst Anja
期刊:Toxins
日期:2020-01-19
DOI :10.3390/toxins12010058
The protein-bound uremic toxins, indoxyl sulfate (IS) and p-cresyl sulfate (PCS), are considered to be harmful vascular toxins. Arterial media calcification, or the deposition of calcium phosphate crystals in the arteries, contributes significantly to cardiovascular complications, including left ventricular hypertrophy, hypertension, and impaired coronary perfusion in the elderly and patients with chronic kidney disease (CKD) and diabetes. Recently, we reported that both IS and PCS trigger moderate to severe calcification in the aorta and peripheral vessels of CKD rats. This review describes the molecular and cellular mechanisms by which these uremic toxins induce arterial media calcification. A complex interplay between inflammation, coagulation, and lipid metabolism pathways, influenced by epigenetic factors, is crucial in IS/PCS-induced arterial media calcification. High levels of glucose are linked to these events, suggesting that a good balance between glucose and lipid levels might be important. On the cellular level, effects on endothelial cells, which act as the primary sensors of circulating pathological triggers, might be as important as those on vascular smooth muscle cells. Endothelial dysfunction, provoked by IS and PCS triggered oxidative stress, may be considered a key event in the onset and development of arterial media calcification. In this review a number of important outstanding questions such as the role of miRNA's, phenotypic switching of both endothelial and vascular smooth muscle cells and new types of programmed cell death in arterial media calcification related to protein-bound uremic toxins are put forward and discussed.
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4区Q2影响因子: 1.3
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12. The Impacts of Sugar-Sweetened Beverages (SSB) on Cardiovascular Health.
期刊:Cureus
日期:2022-07-16
DOI :10.7759/cureus.26908
Cardiovascular disease (CVD) has been a prominent global health challenge in the last decade, and many risk factors and outcomes of CVD have been studied in that timeframe. Recent research has explored the association between sugar-sweetened beverage (SSB) consumption and CVD; however, there is a lack of updated reviews regarding SSB consumption impacts on CVD outcomes and the possible mechanisms affecting the disease state. In turn, this review aims to summarize the relevant published research from the last decade regarding linkages between SSB consumption and CVD outcomes and the potential underlying mechanisms, as well as to highlight opportunities for future exploration with respect to those outcomes and mechanisms. In this review, we searched PubMed, Embase, and Web of Science for peer-reviewed articles published from January 2012 to March 2022 regarding SSB consumption and its association with CVD. The results of our search reveal strong evidence that the consumption of SSB is positively associated with increased risks of CVD and that the magnitude of that risk is increased in a dose-dependent manner. These increased risks range from elevated triglyceride levels to inclined risk of CVD-related mortality. Although the depth of the mechanisms responsible for these increased risks have been less explored thus far, there is some evidence supporting SSB implications in cardiovascular factors, including vascular function, coronary artery calcification, triglyceride levels, inflammatory processes, arterial stiffness, and genetic polymorphisms.
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2区Q1影响因子: 7.6
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13. The common pathobiology between coronary artery disease and calcific aortic stenosis: Evidence and clinical implications.
期刊:Progress in cardiovascular diseases
日期:2023-06-09
DOI :10.1016/j.pcad.2023.06.002
Calcific aortic valve stenosis (CAS), the most prevalent valvular disease worldwide, has been demonstrated to frequently occur in conjunction with coronary artery disease (CAD), the third leading cause of death worldwide. Atherosclerosis has been proven to be the main mechanism involved in CAS and CAD. Evidence also exists that obesity, diabetes, and metabolic syndrome (among others), along with specific genes involved in lipid metabolism, are important risk factors for CAS and CAD, leading to common pathological processes of atherosclerosis in both diseases. Therefore, it has been suggested that CAS could also be used as a marker of CAD. An understanding of the commonalities between the two conditions may improve therapeutic strategies for treating both CAD and CAS. This review explores the common pathogenesis and disparities between CAS and CAD, alongside their etiology. It also discusses clinical implications and provides evidence-based recommendations for the clinical management of both diseases.
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4区Q3影响因子: 1.6
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14. Hemodynamic characteristics and early warnings in very old patients.
作者:Lian Hui , Ding Xin , Zhang Hongmin , Liu Dawei , Wang Xiaoting
期刊:American journal of translational research
日期:2021-12-15
The hemodynamic characteristics of very old patients (VOPs) are unique. With increasing age, patients may experience reduced diastolic function, increased rates of valvular heart disease and coronary atherosclerosis, stiffer vessels, and a reduced heart response to stimulations. Structural and functional modifications are linked to cardiac aging; echocardiography reveals concentric remodeling of the left ventricle, dilation of the left atrium, thickening and calcification of the valves, modification of the large vessels, and abnormal ventricular relaxation. According to a comprehensive understanding of the insufficient compensatory mechanisms of the aging heart, arrythmia should be avoided to the maximum extent and "conservative" fluid therapy should be provided together with appropriate blood pressure control. Considering these factors will improve the success rate of resuscitation and significantly reduce economic loss. In addition, more attention should be paid to the diastolic blood pressure in VOPs.
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3区Q1影响因子: 4.6
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15. Regulation of calcific vascular and valvular disease by nuclear receptors.
期刊:Current opinion in lipidology
日期:2019-10-01
DOI :10.1097/MOL.0000000000000632
PURPOSE OF REVIEW:This review addresses recent developments in studies of lipid regulation of calcific disease of arteries and cardiac valves, including the role of nuclear receptors. The role of lipid-soluble signals and their receptors is timely given the recent evidence and concerns that lipid-lowering treatment may increase the rate of progression of coronary artery calcification, which has been long associated with increased cardiovascular risk. Understanding the mechanisms will be important for interpreting such clinical information. RECENT FINDINGS:New findings support regulation of calcific vascular and valvular disease by nuclear receptors, including the vitamin D receptor, glucocorticoid receptor, nutrient-sensing nuclear receptors (liver X receptor, farnesoid X receptor, and peroxisome proliferator-activated receptors), and sex hormone (estrogen and androgen) receptors. There were two major unexpected findings: first, vitamin D supplementation, which was previously believed to prevent or reduce vascular calcification, showed no cardiovascular benefit in large randomized, controlled trials. Second, both epidemiological studies and coronary intravascular ultrasound studies suggest that treatment with HMG-CoA reductase inhibitors increases progression of coronary artery calcification, raising a question of whether there are mechanically stable and unstable forms of coronary calcification. SUMMARY:For clinical practice and research, these new findings offer new fundamental mechanisms for vascular calcification and provide new cautionary insights for therapeutic avenues.
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3区Q2影响因子: 3.7
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16. NAFLD in Cardiovascular Diseases: A Contributor or Comorbidity?
期刊:Seminars in liver disease
日期:2022-10-14
DOI :10.1055/s-0042-1757712
Nonalcoholic fatty liver disease (NAFLD) and cardiovascular diseases are both highly prevalent conditions around the world, and emerging data have shown an association between them. This review found several longitudinal and cross-sectional studies showing that NAFLD was associated with coronary artery disease, cardiac remodeling, aortic valve remodeling, mitral annulus valve calcifications, diabetic cardiomyopathy, diastolic cardiac dysfunction, arrhythmias, and stroke. Although the specific underlying mechanisms are not clear, many hypotheses have been suggested, including that metabolic syndrome might act as an upstream metabolic defect, leading to end-organ manifestations in both the heart and liver. Management of NAFLD includes weight loss through lifestyle interventions or bariatric surgery, and pharmacological interventions, often targeting comorbidities. Although there are no Food and Drug Administration-approved nonalcoholic steatohepatitis-specific therapies, several drug candidates have demonstrated effect in the improvement in fibrosis or nonalcoholic steatohepatitis resolution. Further studies are needed to assess the effect of those interventions on cardiovascular outcomes, the major cause of mortality in patients with NAFLD. In conclusion, a more comprehensive, multidisciplinary approach to diagnosis and management of patients with NAFLD and cardiovascular diseases is needed to optimize clinical outcomes.
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4区Q3影响因子: 2.1
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17. Towards a new understanding of the molecular mechanisms of cardiovascular disease.
作者:Reis António Heitor
期刊:Discovery medicine
日期:2019-10-01
In this article, we review a process put forward in former publications by which fatty acid micelles and vesicles with an acidic core can develop, and the physiological manifestations of such process in the human body. The process allows the understanding of arterial calcification, why coronary arteries, aorta, and carotids are the most affected vessels, and the preferential distribution of plaques on the areas of the endothelium where shear stress is lower. Also reviewed are the role of systemic buffers in the control of blood pH, and the effects of pollutants, namely heavy metals, diet, and ethanol intake, on cardiovascular risks. The most important cardiovascular risk factors are explained based on their effect on either lowering blood pH or increasing blood FFA concentration, or both. Cardiovascular risk protection factors also find an explanation within the proposed framework. As a final point, the importance of knowing blood pH and concentrations of free fatty acids and albumin concentrations in the blood is emphasized in developing a strategy of prevention of cardiovascular disease.
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3区Q1影响因子: 4.9
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18. Effects of Eicosapentaenoic Acid on Arterial Calcification.
作者:Saito Yukihiro , Nakamura Kazufumi , Ito Hiroshi
期刊:International journal of molecular sciences
日期:2020-07-30
DOI :10.3390/ijms21155455
Arterial calcification is a hallmark of advanced atherosclerosis and predicts cardiovascular events. However, there is no clinically accepted therapy that prevents progression of arterial calcification. HMG-CoA reductase inhibitors, statins, lower low-density lipoprotein-cholesterol and reduce cardiovascular events, but coronary artery calcification is actually promoted by statins. The addition of eicosapentaenoic acid (EPA) to statins further reduced cardiovascular events in clinical trials, JELIS and REDUCE-IT. Additionally, we found that EPA significantly suppressed arterial calcification in vitro and in vivo via suppression of inflammatory responses, oxidative stress and Wnt signaling. However, so far there is a lack of evidence showing the effect of EPA on arterial calcification in a clinical situation. We reviewed the molecular mechanisms of the inhibitory effect of EPA on arterial calcification and the results of some clinical trials.
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4区Q3影响因子: 2.6
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19. Serum biomarkers for arterial calcification in humans: A systematic review.
期刊:Bone reports
日期:2022-06-18
DOI :10.1016/j.bonr.2022.101599
Aim:To clarify the role of mediators of ectopic mineralization as biomarkers for arterial calcifications. Methods:MEDLINE and Embase were searched for relevant literature, until January 4th 2022. The investigated biomarkers were: calcium, phosphate, parathyroid hormone, vitamin D, pyrophosphate, osteoprotegerin, receptor activator of nuclear factor-kappa B ligand (RANKL), fibroblast growth factor-23 (FGF-23), Klotho, osteopontin, osteocalcin, Matrix Gla protein (MGP) and its inactive forms and vitamin K. Studies solely performed in patients with kidney insufficiency or diabetes mellitus were excluded. Results:After screening of 8985 articles, a total of 129 articles were included in this systematic review. For all biomarkers included in this review, the results were variable and more than half of the studies for each specific biomarker had a non-significant result. Also, the overall quality of the included studies was low, partly as a result of the mostly cross-sectional study designs. The largest body of evidence is available for phosphate, osteopontin and FGF-23, as a little over half of the studies showed a significant, positive association. Firm statements for these biomarkers cannot be drawn, as the number of studies was limited and hampered by residual confounding or had non-significant results. The associations of the other mediators of ectopic mineralization with arterial calcifications were not clear. Conclusion:Associations between biomarkers of ectopic mineralization and arterial calcification are variable in the published literature. Future longitudinal studies differentiating medial and intimal calcification could add to the knowledge of biomarkers and mechanisms of arterial calcifications.
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4区Q4影响因子: 1.406
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20. Pathogenesis and Management of Vascular Calcification in Patients with End-Stage Renal Disease.
作者:Ogawa Tetsuya , Nitta Kosaku
期刊:Contributions to nephrology
日期:2018-07-24
DOI :10.1159/000485702
Vascular calcification is common in patients with end-stage renal disease (ESRD). In addition to traditional cardiovascular risk factors, ESRD patients also have a number of nontraditional cardiovascular risk factors that may play an important role in the pathogenesis of vascular calcification. The transformation of vascular smooth muscle cells into osteoblast-like cells may be a key element in the pathogenesis of vascular calcification in the presence of calcium and phosphate deposition due to abnormal bone metabolism and impaired renal excretion. Vascular calcification causes increased arterial stiffness, left ventricular hypertrophy, decreased coronary artery perfusion, myocardial ischemia, and increased cardiovascular morbidity and mortality. Although current treatment strategies focus on correcting abnormal calcium, phosphate, parathyroid hormone, or vitamin D levels in ESRD patients, a better understanding of the mechanisms of abnormal tissue calcification may lead to the development of new therapeutic agents that are capable of reducing vascular calcification and improving the cardiovascular outcome of ESRD patients. This review summarizes the pathogenesis and management of vascular calcification in ESRD patients.
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3区Q3影响因子: 1.3
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21. Warfarin-Induced Calcification: Potential Prevention and Treatment Strategies.
期刊:Reviews in cardiovascular medicine
日期:2022-09-16
DOI :10.31083/j.rcm2309322
Warfarin is clinically used as the first choice for long-term anticoagulant therapy, and for the prevention of thromboembolic events. However, when used at low doses in the long term or high doses in the short term, warfarin treatment may result in tissue calcifications-such as calcifications in the coronary arteries, peripheral vascular system, blood vessels of patients with atrial fibrillation and chronic kidney disease, and vascular valves-and atherosclerotic plaque calcification. These warfarin-induced calcifications may affect cardiovascular function and exacerbate diseases such as diabetes and hypertension. Studies have shown that quercetin, osteoprotegerin, sclerosin, and sodium thiosulfate may alleviate these effects by interfering in the Wnt/ -catenin, TG2/ -catenin, Bone Morphogenetic Protein 2 (BMP2), and Eicosapentaenoic Acid/Matrix Metallopeptidase-9 (EPA/MMP-9) pathways, respectively. Nevertheless, the mechanism underlying warfarin-induced calcification remains unknown. Therefore, the question as to how to effectively attenuate the calcification induced by warfarin and ensure its anticoagulant effect remains an urgent clinical problem that needs to be resolved. To utilize warfarin rationally and to effectively attenuate the calcifications, we focused on the clinical phenomena, molecular mechanisms, and potential strategies to prevent calcification. Highlighting these aspects could provide new insights into the effective utilization of warfarin and the reduction of its associated calcification effects.