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REVIEW article

Front. Cardiovasc. Med.

Sec. Atherosclerosis and Vascular Medicine

Advances in research related to the mechanism of action of the sirtuin family in vascular calcification and its treatment

Provisionally accepted
Zhexue  RenZhexue Ren1Beibei  SongBeibei Song2Yinying  pengYinying peng1Ce  BianCe Bian1Qi  ShenQi Shen1Mengjun  ZhouMengjun Zhou2Bo  LiBo Li2*Xiaodong  JinXiaodong Jin1*
  • 1Shandong Second Medical University, Weifang, China
  • 2Zibo First Hospital, Zibo, China

The final, formatted version of the article will be published soon.

With the acceleration of population aging, the prevalence of vascular calcification (VC) is on the rise, particularly among patients with hypertension, diabetes, chronic kidney disease, and age-related diseases. VC is characterized by the abnormal deposition of calcium phosphate in the vascular walls, and there are currently no effective pharmacological treatments available. This condition is a manifestation of vascular aging. The silent information regulator (SIRT) family, which includes SIRT1 to SIRT7, functions as deacetylases and plays a crucial role in cellular resistance, energy metabolism, apoptosis, and cellular aging, often referred to as longevity proteins. The SIRT family has shown potential in alleviating vascular aging by inhibiting inflammation, reducing endoplasmic reticulum stress, lowering mitochondrial oxidative stress, and promoting DNA damage repair, all of which contribute to the suppression of vascular calcification. Notably, SIRT1, SIRT2, SIRT3, SIRT6, and SIRT7 have demonstrated therapeutic potential in the treatment of vascular calcification.

Keywords: Sirtuin family, Vascular Calcification, vascular smooth muscle cell, Inflammation, Oxidative Stress

Received: 25 Oct 2025; Accepted: 25 Nov 2025.

Copyright: © 2025 Ren, Song, peng, Bian, Shen, Zhou, Li and Jin. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Bo Li
Xiaodong Jin

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