The Role of Autophagy in Osteoarthritic Cartilage

Biomolecules. 2022 Sep 23;12(10):1357. doi: 10.3390/biom12101357.

Abstract

Osteoarthritis (OA) is one of the most common diseases leading to physical disability, with age being the main risk factor, and degeneration of articular cartilage is the main focus for the pathogenesis of OA. Autophagy is a crucial intracellular homeostasis system recycling flawed macromolecules and cellular organelles to sustain the metabolism of cells. Growing evidences have revealed that autophagy is chondroprotective by regulating apoptosis and repairing the function of damaged chondrocytes. Then, OA is related to autophagy depending on different stages and models. In this review, we discuss the character of autophagy in OA and the process of the autophagy pathway, which can be modulated by some drugs, key molecules and non-coding RNAs (microRNAs, long non-coding RNAs and circular RNAs). More in-depth investigations of autophagy are needed to find therapeutic targets or diagnostic biomarkers through in vitro and in vivo situations, making autophagy a more effective way for OA treatment in the future. The aim of this review is to introduce the concept of autophagy and make readers realize its impact on OA. The database we searched in is PubMed and we used the keywords listed below to find appropriate article resources.

Keywords: AMP-activated protein kinase (AMPK); Autophagy; Osteoarthritis (OA); circular RNAs; long non-coding RNAs; microRNAs; non-coding RNAs.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / physiology
  • Autophagy / physiology
  • Biomarkers / metabolism
  • Cartilage, Articular*
  • Humans
  • MicroRNAs* / metabolism
  • Osteoarthritis* / pathology
  • RNA, Circular

Substances

  • RNA, Circular
  • MicroRNAs
  • Biomarkers

Grants and funding

This study was supported in part by the National Health Research Institute (NHRI-EX101-9935EI) of Taiwan, Kaohsiung Medical University (NPUST-KMU-109-P002, NCTUKMU108-BIO-04, KMU-TC108A02-1, KMU-DK105009, KMU-DK(B) 110002 and KMU-111-P005), Kaohsiung Municipal Ta-Tung Hospital (KMTTH-109-R014, KMTTH-DK(B) 110002-1 and KMTTH-110-R008), and the Minister of Science and Technology of Taiwan (MOST 110-2314-B-006-037-MY3, 108-2314-B-037-059-MY3, 110-2314-B-037-029-MY3 and 111-2314-B-037-106-). The funders had no role in the study design, data collection, and analysis, decision to publish, or preparation of the manuscript.