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血管生长因子增多,血管平滑肌细胞增殖和炎症在血管重塑方面起到了关键的作用。这种低级的炎症反应导致粘附分子表达,白细胞的侵入,细胞因子的产生,氧化应激的增加,从而激活免疫细胞和血管炎症信号通路,使T淋巴细胞及巨噬细胞等细胞活化,产生和释放多种活性因子,激活心肌的细胞外基质生成细胞,引起胶原形成及代谢异常,并可导致心肌实质细胞的变性、坏死或亚细胞结构变化等,从而引起心肌纤维化一系列病理生理变化。本文主要就CD8+T淋巴细胞在高血压心肌纤维化炎症反应中的细胞毒性作用、诱导细胞凋亡作用、分泌大量的炎症因子、增加MMPs的活性从而影响心肌纤维化的形成等方面做一综述!
Increased vascular growth factor, vascular smooth muscle cell proliferation and inflammation play a key role in vascular remodeling. This low level of inflammatory response leads to the expression of adhesion molecules, the invasion of leukocytes, the production of cytokines, and the increase of oxidative stress, thereby activating immune cells and vascular inflammatory signaling pathways, activating cells such as T lymphocytes and macrophages, And release a variety of active factors, activate the extracellular matrix of myocardial cells to generate cells, causing collagen formation and metabolic abnormalities, and can lead to myocardial degeneration, necrosis or subcellular structural changes, resulting in a series of pathophysiological changes in myocardial fibrosis . This review summarizes the cytotoxicity of CD8 + T lymphocytes in the inflammatory reaction of hypertensive myocardial fibrosis, the induction of apoptosis, the secretion of a large number of inflammatory cytokines, the increase of the activity of MMPs and the formation of myocardial fibrosis !