منابع مشابه
Vascular endothelial senescence: from mechanisms to pathophysiology.
Most mitotically competent mammalian cell types can react to stress by undergoing a phenotypically distinctive and permanent form of growth arrest called "cellular senescence." This response has been extensively characterized in cell culture and more recently it has been found to occur also in vivo in a number of tissues. In this review I will present the case for the occurrence of senescence i...
متن کاملIncreased vascular senescence and impaired endothelial progenitor cell function mediated by mutation of circadian gene Per2.
BACKGROUND Alteration of the circadian rhythm and increased vascular senescence are linked to cardiovascular disease. Per2, a circadian gene, is known to regulate endothelium-dependent vasomotion. However, the mechanism by which Per2 affects endothelial function is unknown. We hypothesize that endothelial dysfunction in Per2 mutant (Per2(m/m)) mice is mediated in part by increased vascular sene...
متن کاملVascular smooth muscle cell senescence in atherosclerosis.
Markers of cell senescence have been identified in both the blood and vessel wall of patients with atherosclerosis. In particular, vascular smooth muscle cells (VSMCs) derived from human plaques show numerous features of senescence both in culture and in vivo. This review summarises the evidence for VSMC senescence in atherosclerosis, and outlines the mechanisms and triggers leading to their se...
متن کاملMicroparticles Induce Cell Cycle Arrest Through Redox-Sensitive Processes in Endothelial Cells: Implications in Vascular Senescence
BACKGROUND Chronic disease accelerates endothelial dysfunction in aging, a process associated with cell senescence. However, the mechanisms underlying this process are unclear. We examined whether endothelial cell (EC)-derived microparticles (MPs) facilitate EC senescence and questioned the role of reactive oxygen species in this process. METHODS AND RESULTS Senescence was induced by sequenti...
متن کاملHepatocyte growth factor, but not vascular endothelial growth factor, attenuates angiotensin II-induced endothelial progenitor cell senescence.
Although both hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) are potent angiogenic growth factors in animal models of ischemia, their characteristics are not the same in animal experiments and clinical trials. To elucidate the discrepancy between HGF and VEGF, we compared the effects of HGF and VEGF on endothelial progenitor cells under angiotensin II stimulation, ...
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ژورنال
عنوان ژورنال: Japanese Journal of Thrombosis and Hemostasis
سال: 2019
ISSN: 0915-7441,1880-8808
DOI: 10.2491/jjsth.30.521