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Necroptosis in the periodontal homeostasis: Signals emanating from dying cells. Li J,Ke X,Yan F,Lei L,Li H Oral diseases Periodontal tissues are constantly exposed to microbial stimuli. The equilibrium between microbes and host defense system helps maintain the homeostasis in the periodontal microenvironment. Growth of pathogenic bacteria in dental biofilms may induce proinflammatory cytokine production to recruit sentinel cells, mainly neutrophils and monocytes into the gingival sulcus or the periodontal pocket. Moreover, dysbiosis with overgrowth of anaerobic pathogens, such as Porphyromonas gingivalis and Tannerella forsythia, may induce death of both immune cells and host resident cells. Necroptosis is one newly characterized programmed cell death mediated by receptor-interacting protein kinase (RIPK)-1, RIPK3, and mixed lineage kinase like (MLKL). With its release of death-associated molecular patterns (DAMPs) into extracellular environment, necroptosis may help transmit the danger signal and amplify the inflammatory responses. In this review, we present recent advances on how necroptosis influences bacterial infection progression and what a role necroptosis plays in maintaining the homeostasis in the periodontal niche. Until we fully decipher the signals emanated from dying cells, we cannot completely understand the mechanism of disease progression. 10.1111/odi.12722
Anaemia, iron homeostasis and pulmonary hypertension: a review. Sonnweber Thomas,Pizzini Alex,Tancevski Ivan,Löffler-Ragg Judith,Weiss Günter Internal and emergency medicine Anaemia is a highly prevalent condition, which negatively impacts on patients' cardiovascular performance and quality of life. Anaemia is mainly caused by disturbances of iron homeostasis. While absolute iron deficiency mostly as a consequence of chronic blood loss or insufficient dietary iron absorption results in the emergence of iron deficiency anaemia, inflammation-driven iron retention in innate immune cells and blockade of iron absorption leads to the development of anaemia of chronic disease. Both, iron deficiency and anaemia have been linked to the clinical course of pulmonary hypertension. Various mechanistic links between iron homeostasis, anaemia, and pulmonary hypertension have been described and current treatment guidelines suggest regular iron status assessment and the implementation of iron supplementation strategies in these patients. The pathophysiology, diagnostic assessment as well as current and future treatment options concerning iron deficiency with or without anaemia in individuals suffering from pulmonary hypertension are discussed within this review. 10.1007/s11739-020-02288-1
Critical COVID-19 disease, homeostasis, and the "surprise" of effective glucocorticoid therapy. Chrousos George P,Meduri G Umberto Clinical immunology (Orlando, Fla.) 10.1016/j.clim.2020.108550
Homeostasis, inflammation, and disease susceptibility. Kotas Maya E,Medzhitov Ruslan Cell While modernization has dramatically increased lifespan, it has also witnessed the increasing prevalence of diseases such as obesity, hypertension, and type 2 diabetes. Such chronic, acquired diseases result when normal physiologic control goes awry and may thus be viewed as failures of homeostasis. However, while nearly every process in human physiology relies on homeostatic mechanisms for stability, only some have demonstrated vulnerability to dysregulation. Additionally, chronic inflammation is a common accomplice of the diseases of homeostasis, yet the basis for this connection is not fully understood. Here we review the design of homeostatic systems and discuss universal features of control circuits that operate at the cellular, tissue, and organismal levels. We suggest a framework for classification of homeostatic signals that is based on different classes of homeostatic variables they report on. Finally, we discuss how adaptability of homeostatic systems with adjustable set points creates vulnerability to dysregulation and disease. This framework highlights the fundamental parallels between homeostatic and inflammatory control mechanisms and provides a new perspective on the physiological origin of inflammation. 10.1016/j.cell.2015.02.010