Key Lab of Medical Electrophysiology of Ministry of Education and Medical Electrophysiological Key Lab of Sichuan Province, Collaborative Innovation Center for Prevention and Treatment of Cardiovascular Disease, Institute of Cardiovascular Research, Public Center of Experimental Technology, Hemodynamics and Medical Engineering Combination Key Laboratory of Luzhou, Southwest Medical University, Luzhou, China.
Channels (Austin). 2024 Dec;18(1):2418128. doi: 10.1080/19336950.2024.2418128. Epub 2024 Oct 19.
Fibrosis is usually the final pathological state of many chronic inflammatory diseases and may lead to organ malfunction. Excessive deposition of extracellular matrix (ECM) molecules is a characteristic of most fibrotic tissues. The blood vessel wall contains three layers of membrane structure, including the intima, which is composed of endothelial cells; the media, which is composed of smooth muscle cells; and the adventitia, which is formed by the interaction of connective tissue and fibroblasts. The occurrence and progression of vascular remodeling are closely associated with cardiovascular diseases, and vascular remodeling can alter the original structure and function of the blood vessel. Dysregulation of the composition of the extracellular matrix in blood vessels leads to the continuous advancement of vascular stiffening and fibrosis. Vascular fibrosis reaction leads to excessive deposition of the extracellular matrix in the vascular adventitia, reduces vessel compliance, and ultimately alters key aspects of vascular biomechanics. The pathogenesis of fibrosis in the vasculature and strategies for its reversal have become interesting and important challenges. Ion channels are widely expressed in the cardiovascular system; they regulate blood pressure, maintain cardiovascular function homeostasis, and play important roles in ion transport, cell differentiation, proliferation. In blood vessels, different types of ion channels in fibroblasts, smooth muscle cells and endothelial cells may be relevant mediators of the development of fibrosis in organs or tissues. This review discusses the known roles of ion channels in vascular fibrosis remodeling and discusses potential therapeutic targets for regulating remodeling and repair after vascular injury.
纤维化通常是许多慢性炎症性疾病的最终病理状态，可能导致器官功能障碍。细胞外基质（ECM）分子的过度沉积是大多数纤维化组织的特征。血管壁包含三层膜结构，包括内膜，由内皮细胞组成；中膜，由平滑肌细胞组成；和外膜，由结缔组织和成纤维细胞相互作用形成。血管重塑的发生和进展与心血管疾病密切相关，血管重塑可以改变血管的原始结构和功能。血管细胞外基质组成的失调导致血管僵硬和纤维化的不断进展。血管纤维化反应导致血管外膜中细胞外基质的过度沉积，降低了血管顺应性，最终改变了血管生物力学的关键方面。血管纤维化的发病机制及其逆转策略已成为一个有趣且重要的挑战。离子通道在心血管系统中广泛表达；它们调节血压，维持心血管功能的稳态，并在离子转运、细胞分化、增殖等方面发挥重要作用。在血管中，成纤维细胞、平滑肌细胞和内皮细胞中的不同类型的离子通道可能是器官或组织纤维化发展的相关介质。本综述讨论了已知的离子通道在血管纤维化重塑中的作用，并讨论了调节血管损伤后重塑和修复的潜在治疗靶点。
