The intervertebral disc and cartilage are specialized, extracellular matrix-rich tissues critical for absorbing mechanical loads, providing flexibility to the joints, and longitudinal growth in the case of growth plate cartilage. Specialized niche conditions in these tissues, such as hypoxia, are critical in regulating cellular activities including autophagy, a lysosomal degradation pathway that promotes cell survival. Mounting evidence suggests that dysregulation of autophagic pathways underscores many skeletal pathologies affecting the spinal column, articular and growth plate cartilages. Many lysosomal storage disorders characterized by the accumulation of partially degraded glycosaminoglycans (GAGs) due to the lysosomal dysfunction thus affect skeletal tissues and result in altered ECM structure. Likewise, pathologies that arise from mutations in genes encoding ECM proteins and ECM processing, folding, and post-translational modifications, result in accumulation of misfolded proteins in the ER, ER stress and autophagy dysregulation. These conditions evidence reduced secretion of ECM proteins and/or increased secretion of mutant proteins, thereby impairing matrix quality and the integrity of affected skeletal tissues and causing a lack of growth and degeneration. In this review, we discuss the role of autophagy and mechanisms of its regulation in the intervertebral disc and cartilages, as well as how dysregulation of autophagic pathways affects these skeletal tissues.

椎间盘和软骨是专门的、富含细胞外基质的组织，对于吸收机械负荷、为关节提供灵活性以及生长板软骨的纵向生长至关重要。这些组织中的特殊生态位条件（例如缺氧）对于调节细胞活动至关重要，包括自噬，这是一种促进细胞存活的溶酶体降解途径。越来越多的证据表明，自噬通路的失调强调了许多影响脊柱、关节和生长板软骨的骨骼病变。由于溶酶体功能障碍，许多以部分降解的糖胺聚糖 (GAG) 积累为特征的溶酶体贮积症会影响骨骼组织并导致 ECM 结构改变。同样地，由编码 ECM 蛋白和 ECM 加工、折叠和翻译后修饰的基因突变引起的病理，导致错误折叠蛋白在内质网中的积累、内质网应激和自噬失调。这些情况表明 ECM 蛋白分泌减少和/或突变蛋白分泌增加，从而损害基质质量和受影响骨骼组织的完整性，并导致缺乏生长和退化。在这篇综述中，我们讨论了自噬在椎间盘和软骨中的作用及其调节机制，以及自噬通路的失调如何影响这些骨骼组织。ER应激和自噬失调。这些情况表明 ECM 蛋白分泌减少和/或突变蛋白分泌增加，从而损害基质质量和受影响骨骼组织的完整性，并导致缺乏生长和退化。在这篇综述中，我们讨论了自噬在椎间盘和软骨中的作用及其调节机制，以及自噬通路的失调如何影响这些骨骼组织。ER应激和自噬失调。这些情况表明 ECM 蛋白分泌减少和/或突变蛋白分泌增加，从而损害基质质量和受影响骨骼组织的完整性，并导致缺乏生长和退化。在这篇综述中，我们讨论了自噬在椎间盘和软骨中的作用及其调节机制，以及自噬通路的失调如何影响这些骨骼组织。