2. Academic Validation
  3. Curcumin improves diabetic vascular aging rats and high glucose-induced cells aging by promoting mitophagy

Curcumin improves diabetic vascular aging rats and high glucose-induced cells aging by promoting mitophagy

  • 3 Biotech. 2025 Oct;15(10):341. doi: 10.1007/s13205-025-04510-3.
Jinlin Wu # 1 2,  Xi Mei # 3 2,  Yong Li 1,  Fang Liu 1,  Dongfang Liu 2
Affiliations

Affiliations

  • 1 Department of Endocrinology and Metabolism, Chongqing Traditional Chinese Medicine Hospital, The First Affiliated Hospital of Chongqing University of Chinese Medicine, Chongqing, 400021 China.
  • 2 Department of Endocrinology and Metabolism, The Second Affiliated Hospital, Chongqing Medical University, No. 74 Linjiang Road, Yuzhong District, Chongqing, 400010 China.
  • 3 Department of Endocrinology and Metabolism, The First Affiliated Hospital of Chengdu Medical College, Chengdu, 610500 Sichuan China.
  • # Contributed equally.
PMID: 40951878 DOI: 10.1007/s13205-025-04510-3
Abstract

Vascular aging was reported to be closely related to diabetes. This study investigates the inhibitory effects and mechanism of curcumin on diabetic vascular aging by regulating Mitophagy through the PINK1 pathway. The diabetic rat model was established by feeding with a high-fat diet and intraperitoneal injection of streptozotocin (STZ), and treated with high-dose (200 mg/kg), low-dose (50 mg/kg) curcumin, or metformin (200 mg/kg), respectively. The role of Mitophagy in high glucose (HG)-induced human aortic smooth muscle cells (HASMCs) aging in vitro were investigated. The results indicated that curcumin ameliorated weight loss and improved elevated blood glucose levels in diabetic rats. Curcumin also improved the vascular pathological changes of the common carotid artery, decreased the vascular interstitial Collagen fiber and vascular calcium salt deposition, and improved vascular ultrastructure. Furthermore, curcumin significantly decreased ET-1, VCAM-1, and p16 expressions. In addition, curcumin increased the expression of LC3II/I, Beclin1, and PINK1 proteins, while decreasing p62 expression. High-dose curcumin could improve mitochondrial morphology and increase mitochondrial Autophagy. Additionally, curcumin increased HASMCs viability and inhibited HG-induced vascular aging by promoting Mitophagy in vitro. WB confirmed that LC3II/I, Beclin1, and PINK1 levels were increased, while p62 and p16 levels were decreased. The improvement effect of curcumin on vascular aging was reversed by the Mitophagy inhibitor Mdivi-1 or PINK1 siRNA. In conclusion, curcumin alleviates vascular aging in diabetic rats and HG-induced senescence in HASMCs by enhancing mitochondrial Autophagy. These results suggest that curcumin has therapeutic potential in alleviating diabetic vascular aging.

Supplementary information: The online version contains supplementary material available at 10.1007/s13205-025-04510-3.

Keywords

Curcumin; Diabetes; Mitophagy; PINK1; Vascular aging.

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