关键词: cardiovascular disease inflammation vascular remodelling

Mesh : Humans Vascular Remodeling Inflammation / metabolism Cardiovascular Diseases / physiopathology metabolism Hypertension / physiopathology metabolism Animals Oxidative Stress Signal Transduction Oxidation-Reduction

来  源:   DOI:10.1042/CS20220797

Abstract:
Optimal vascular structure and function are essential for maintaining the physiological functions of the cardiovascular system. Vascular remodelling involves changes in vessel structure, including its size, shape, cellular and molecular composition. These changes result from multiple risk factors and may be compensatory adaptations to sustain blood vessel function. They occur in diverse cardiovascular pathologies, from hypertension to heart failure and atherosclerosis. Dynamic changes in the endothelium, fibroblasts, smooth muscle cells, pericytes or other vascular wall cells underlie remodelling. In addition, immune cells, including macrophages and lymphocytes, may infiltrate vessels and initiate inflammatory signalling. They contribute to a dynamic interplay between cell proliferation, apoptosis, migration, inflammation, and extracellular matrix reorganisation, all critical mechanisms of vascular remodelling. Molecular pathways underlying these processes include growth factors (e.g., vascular endothelial growth factor and platelet-derived growth factor), inflammatory cytokines (e.g., interleukin-1β and tumour necrosis factor-α), reactive oxygen species, and signalling pathways, such as Rho/ROCK, MAPK, and TGF-β/Smad, related to nitric oxide and superoxide biology. MicroRNAs and long noncoding RNAs are crucial epigenetic regulators of gene expression in vascular remodelling. We evaluate these pathways for potential therapeutic targeting from a clinical translational perspective. In summary, vascular remodelling, a coordinated modification of vascular structure and function, is crucial in cardiovascular disease pathology.
摘要:
最佳的血管结构和功能对于维持心血管系统的生理功能至关重要。血管重塑涉及血管结构的变化,包括它的大小,形状,细胞和分子组成。这些变化是由多种危险因素引起的,可能是维持血管功能的代偿适应。它们发生在不同的心血管疾病中,从高血压到心力衰竭和动脉粥样硬化。内皮的动态变化,成纤维细胞,平滑肌细胞,周细胞或其他血管壁细胞在重塑的基础上。此外,免疫细胞,包括巨噬细胞和淋巴细胞,可能渗入血管并启动炎症信号。它们有助于细胞增殖之间的动态相互作用,凋亡,迁移,炎症,和细胞外基质重组,血管重塑的所有关键机制。这些过程背后的分子途径包括生长因子(例如,血管内皮生长因子和血小板衍生生长因子),炎性细胞因子(例如,白细胞介素-1β和肿瘤坏死因子-α),活性氧,和信号通路,如Rho/ROCK,MAPK,和TGF-β/Smad,与一氧化氮和超氧化物生物学有关。MicroRNA和长链非编码RNA是血管重塑中基因表达的重要表观遗传调节因子。我们从临床转化的角度评估了这些潜在的治疗靶向途径。总之,血管重塑,血管结构和功能的协调改变,在心血管疾病病理学中至关重要。
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