Fibrosis is characterized by excessive deposition of extracellular matrix components such as collagen in tissues or organs. Fibrosis can develop in the heart, kidneys, liver, skin or any other body organ in response to injury or maladaptive reparative processes, reducing overall function and leading eventually to organ failure. A variety of cellular and molecular signaling mechanisms are involved in the pathogenesis of fibrosis. The renin-angiotensin-aldosterone system (RAAS) interacts with the potent Transforming Growth Factor β (TGFβ) pro-fibrotic pathway to mediate fibrosis in many cell and tissue types. RAAS consists of both classical and alternative pathways, which act to potentiate or antagonize fibrotic signaling mechanisms, respectively. This review provides an overview of recent literature describing the roles of RAAS in the pathogenesis of fibrosis, particularly in the liver, heart, kidney and skin, and with a focus on RAAS interactions with TGFβ signaling. Targeting RAAS to combat fibrosis represents a promising therapeutic approach, particularly given the lack of strategies for treating fibrosis as its own entity, thus animal and clinical studies to examine the impact of natural and synthetic substances to alter RAAS signaling as a means to treat fibrosis are reviewed as well.

纤维化的特征在于细胞外基质成分如胶原蛋白在组织或器官中的过度沉积。纤维化可在心脏、肾脏、肝脏、皮肤或任何其他身体器官中发生，以应对损伤或适应不良的修复过程，从而降低整体功能并最终导致器官衰竭。纤维化的发病机制涉及多种细胞和分子信号传导机制。肾素-血管紧张素-醛固酮系统 (RAAS) 与有效的转化生长因子 β (TGFβ) 促纤维化途径相互作用，在许多细胞和组织类型中介导纤维化。RAAS 由经典和替代途径组成，分别用于增强或拮抗纤维化信号传导机制。本综述概述了近期文献，这些文献描述了 RAAS 在纤维化发病机制中的作用，特别是在肝脏、心脏、肾脏和皮肤中，并重点关注 RAAS 与 TGFβ 信号传导的相互作用。靶向 RAAS 来对抗纤维化代表了一种很有前景的治疗方法，特别是考虑到缺乏将纤维化作为其自身实体治疗的策略，因此动物和临床研究以检查天然和合成物质对改变 RAAS 信号的影响作为治疗纤维化的一种手段是也进行了审查。