Mechanistic insights into non-coding RNAs regulate autophagy in chondrocytes and their contribution to osteoarthritis

TL;DR

This paper reviews how non-coding RNAs regulate autophagy in cartilage cells, contributing to osteoarthritis development.

Contribution

The paper provides new insights into the regulatory mechanisms of non-coding RNAs in autophagy and osteoarthritis.

Findings

Non-coding RNAs influence autophagy in chondrocytes through post-transcriptional and epigenetic mechanisms.

There is a crucial interplay between non-coding RNAs, autophagy, and osteoarthritis pathogenesis.

Understanding these mechanisms could lead to novel therapeutic targets for osteoarthritis.

Abstract

Osteoarthritis (OA), a chronic degenerative joint disease, arises from a confluence of factors including aging, mechanical injury, and obesity. Autophagy, a fundamental cellular process involving the degradation and recycling of cellular components, plays a critical role in chondrocyte homeostasis and survival under stress. Non-coding RNAs (ncRNAs), a diverse class of RNA molecules with no protein-coding potential, exert significant influence on gene expression through post-transcriptional and epigenetic mechanisms. Growing evidence suggests a crucial interplay between ncRNAs, autophagy, and OA pathogenesis. This review summarizes the multifaceted role of autophagy in OA chondrocytes and delves into the regulatory mechanisms of ncRNAs on OA-associated autophagy, aiming to elucidate the intricate pathological network underlying OA development and identify novel therapeutic targets.

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