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Role of mitophagy in intervertebral disc degeneration: A narrative review

Zuo-Long Wu1, Yong Liu1, Wei Song1

  • 1Department of Orthopedics, The Second Hospital&Clinical Medical School, Lanzhou University, Lanzhou, China; Orthopaedics Key Laboratory of Gansu Province, The Second Hospital&Clinical Medical School, Lanzhou University, Lanzhou, China; The Cuiying Biomedical Research Center, The Second Hospital&Clinical Medical School, Lanzhou University, Lanzhou, China.

Osteoarthritis and Cartilage
|November 13, 2024
PubMed
Abstract

Insights

Mitophagy, a cellular process, plays a dual role in intervertebral disc degeneration (IDD). Proper mitophagy maintains disc health, while excessive mitophagy accelerates IDD progression.

Area of Science:

  • Cell Biology
  • Biomedical Science
  • Pathogenesis Research

Background:

  • Intervertebral disc degeneration (IDD) is a significant health concern.
  • Mitophagy's role in IDD pathogenesis is increasingly recognized.
  • Understanding mitophagy is key to developing new IDD treatments.

Purpose of the Study:

  • To review the regulatory mechanisms of mitophagy.
  • To summarize mitophagy's role in IDD.
  • To explore therapeutic strategies targeting mitophagy for IDD.

Main Methods:

  • This study is a narrative review.
  • It synthesizes current research on mitophagy and IDD.
  • The review covers regulatory mechanisms, IDD roles, and therapeutic prospects.

Main Results:

  • Mitophagy protects against cellular damage and promotes extracellular matrix (ECM) production.
  • It inhibits ECM degradation, apoptosis, senescence, and calcification.
  • However, excessive mitophagy can be detrimental, with regulatory mechanisms unclear.

Conclusions:

  • Appropriate mitophagy maintains intervertebral disc cell homeostasis and slows IDD.
  • Excessive mitophagy may accelerate IDD.
  • Further research into mitophagy regulation is crucial for effective IDD therapies.
Keywords:
Autophagy lysosomesIntervertebral discIntervertebral disc degenerationMitophagyNucleus pulposus

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