Metformin prevents the onset and progression of intervertebral disc degeneration: New insights and potential mechanisms (Review)

Int J Mol Med. 2024 Aug;54(2):71. doi: 10.3892/ijmm.2024.5395. Epub 2024 Jul 4.

Abstract

Metformin has been the go‑to medical treatment for addressing type 2 diabetes mellitus (T2DM) as a frontline oral antidiabetic. Obesity, cancer and bone deterioration are linked to T2DM, which is considered a metabolic illness. Numerous diseases associated with T2DM, such as tumours, cardiovascular disease and bone deterioration, may be treated with metformin. Intervertebral disc degeneration (IVDD) is distinguished by degeneration of the spinal disc, accompanied by the gradual depletion of proteoglycans and water in the nucleus pulposus (NP) of the IVD, resulting in lower back pain. The therapeutic effect of metformin on IVDD has also attracted much attention. By stimulating AMP‑activated kinase, metformin could enhance autophagy and suppress cell senescence, apoptosis and inflammation, thus effectively delaying IVDD. The present review aimed to systematically explain the development of IVDD and mechanism of metformin in the treatment and prevention of IVDD to provide a reference for the clinical application of metformin as adjuvant therapy in the treatment of IVDD.

Keywords: intervertebral disc degeneration; nucleus pulposus; mechanism; metformin; treatment; type 2 diabetes mellitus.

Publication types

  • Review

MeSH terms

  • Animals
  • Autophagy / drug effects
  • Diabetes Mellitus, Type 2 / drug therapy
  • Diabetes Mellitus, Type 2 / metabolism
  • Disease Progression
  • Humans
  • Hypoglycemic Agents / pharmacology
  • Hypoglycemic Agents / therapeutic use
  • Intervertebral Disc Degeneration* / drug therapy
  • Intervertebral Disc Degeneration* / metabolism
  • Intervertebral Disc Degeneration* / prevention & control
  • Metformin* / pharmacology
  • Metformin* / therapeutic use
  • Nucleus Pulposus / drug effects
  • Nucleus Pulposus / metabolism
  • Nucleus Pulposus / pathology

Substances

  • Metformin
  • Hypoglycemic Agents

Grants and funding

The present study was supported by the National Natural Science Foundation of China (grant no. 82072492) and the Excellent Youth Scientific Research Projects in Anhui Universities (grant no. 2022AH030117).