Metformin ameliorates valve interstitial cell calcification by promoting autophagic flux

Sci Rep. 2023 Dec 5;13(1):21435. doi: 10.1038/s41598-023-47774-6.

Abstract

Calcific aortic valve disease (CAVD) is the most common heart disease of the developed world. It has previously been established that metformin administration reduces arterial calcification via autophagy; however, whether metformin directly regulates CAVD has yet to be elucidated. In the present study we investigated whether metformin alleviates valvular calcification through the autophagy-mediated recycling of Runx2. Calcification was reduced in rat valve interstitial cells (RVICs) by metformin treatment (0.5-1.5 mM) (P < 0.01), with a marked decrease in Runx2 protein expression compared to control cells (P < 0.05). Additionally, upregulated expression of Atg3 and Atg7 (key proteins required for autophagosome formation), was observed following metformin treatment (1 mM). Blocking autophagic flux using Bafilomycin-A1 revealed colocalisation of Runx2 with LC3 puncta in metformin treated RVICs (P < 0.001). Comparable Runx2 accumulation was seen in LC3 positive autolysosomes present within cells that had been treated with both metformin and hydroxychloroquine in combination (P < 0.001). Mechanistic studies employing three-way co-immunoprecipitation with Runx2, p62 and LC3 suggested that Runx2 binds to LC3-II upon metformin treatment in VICs. Together these studies suggest that the utilisation of metformin may represent a novel strategy for the treatment of CAVD.

MeSH terms

  • Animals
  • Aortic Valve Stenosis* / drug therapy
  • Aortic Valve Stenosis* / metabolism
  • Autophagy
  • Cells, Cultured
  • Core Binding Factor Alpha 1 Subunit / genetics
  • Metformin* / pharmacology
  • Rats

Substances

  • Core Binding Factor Alpha 1 Subunit
  • Metformin

Supplementary concepts

  • Aortic Valve, Calcification of