Autophagy is a very versatile process through which the cell degrades damaged long-lived proteins, entire organelles, or pathogens, by engulfing them in characteristic double-membrane vesicles and conveying the cargo to lysosomes. It is a dynamic pathway tunable at multiple levels and responsive to nutrient and stress stimuli, also coming from the extracellular microenvironment and its remodeling. In the extracellular matrix, collagen type VI forms a distinctive set of beaded microfilaments that assemble into an intricate and multimodular meshwork of tightly linked proteins and surface receptors. When missing or defective, collagen VI triggers a series of pathological events in skeletal muscle and other tissues, with a remarkable impact on key cell processes, such as apoptosis and autophagy. In this review, we discuss the current knowledge about collagen VI regulation of autophagy in the different experimental models and human pathologies where it was studied, and provide some hints for future directions aimed at the fine dissection of this intriguing relationship, as well as its prospective translational impact for disease and therapy.

自噬是一个非常通用的过程，通过该过程，细胞通过将受损的长寿命蛋白质、整个细胞器或病原体吞噬在特征性的双膜囊泡中并将其运送到溶酶体中来降解它们。它是一种动态途径，可在多个水平上调节，对营养和压力刺激有反应，也来自细胞外微环境及其重塑。在细胞外基质中，VI 型胶原蛋白形成一组独特的珠状微丝，这些微丝组装成一个由紧密连接的蛋白质和表面受体组成的错综复杂的多模块网状结构。当缺失或缺陷时，VI 型胶原蛋白会引发骨骼肌和其他组织中的一系列病理事件，对细胞凋亡和自噬等关键细胞过程产生显着影响。在本次审查中，