Tissue repair and fibrosis, an abnormal form of repair, occur in most human organs in response to injury or inflammation. Fibroblasts play a major role in the normal repair process by differentiating into myofibroblasts that synthesize extracellular matrix (ECM) components and favor tissue remodeling to reestablish normal function and integrity. However, their persistent accumulation at the site of injury is a hallmark of fibrosis. Autophagy is a catabolic process that occurs in eukaryotic cells as a stress response to allow cell survival and maintenance of cellular homeostasis by degrading and recycling intracellular components. Recent advances identify autophagy as an important regulator of myofibroblast differentiation, tissue remodeling, and fibrogenesis. In this mini-review, we provide an overview of the interactions between autophagy, ECM, and fibrosis, and emphasize the molecular mechanisms involved in myofibroblast differentiation. We also describe the emerging concept of secretory autophagy as a new avenue for intercellular communication at the site of tissue injury and repair.

组织修复和纤维化是一种异常的修复形式，发生在大多数人体器官中，以应对损伤或炎症。成纤维细胞通过分化为合成细胞外基质 (ECM) 成分并有利于组织重塑以重建正常功能和完整性的肌成纤维细胞，在正常修复过程中发挥重要作用。然而，它们在损伤部位的持续积累是纤维化的标志。自噬是真核细胞中发生的分解代谢过程，作为一种应激反应，通过降解和回收细胞内成分来允许细胞存活和维持细胞稳态。最近的进展将自噬确定为肌成纤维细胞分化、组织重塑和纤维发生的重要调节因子。在这篇小型评论中，我们概述了自噬、ECM、和纤维化，并强调参与肌成纤维细胞分化的分子机制。我们还将新兴的分泌性自噬概念描述为组织损伤和修复部位细胞间通讯的新途径。