Non-coding RNAs regulating autophagy in Osteoporosis: mechanistic insights and therapeutic potential

Osteoporosis (OP) is a systemic skeletal disease, defined by low bone mass and microarchitectural deterioration of bone, which increases the risk of fragility fractures. Autophagy is a dynamic and evolutionarily conserved process that regulates the degradation and recycling of cellular proteins and organelles in response to various physiological and pathophysiological conditions. Autophagy is a major stress-response pathway and it is critically involved in regulating the metabolic and homeostatic functions of bone cells. Non-coding RNAs (ncRNAs) are a diverse group of RNAs that do not code for proteins, but act as post-transcriptional and epigenetic modulators of gene expression, and thus play an important role in diverse biological processes. Accumulating evidence suggests that ncRNA-autophagy networks contribute to the development of OP. In this review, we summarize the mechanisms by which ncRNAs regulate autophagy and outline the roles of autophagy in osteoclasts, osteoblasts, bone marrow mesenchymal stem cells, and osteocytes. We further discuss the mechanistic roles of ncRNA-autophagy axes in OP pathogenesis and potential therapeutic strategies targeting these axes.