Volume 24 Issue 3
Mar.  2026
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CAI Fengjiao, WU Jinhong, WANG Lili, MA Yichao, LU Yan. The role of TRIM62 in regulating autophagy in aortic smooth muscle cells through the mTOR pathway[J]. Chinese Journal of General Practice, 2026, 24(3): 395-398. doi: 10.16766/j.cnki.issn.1674-4152.004404
Citation: CAI Fengjiao, WU Jinhong, WANG Lili, MA Yichao, LU Yan. The role of TRIM62 in regulating autophagy in aortic smooth muscle cells through the mTOR pathway[J]. Chinese Journal of General Practice, 2026, 24(3): 395-398. doi: 10.16766/j.cnki.issn.1674-4152.004404

The role of TRIM62 in regulating autophagy in aortic smooth muscle cells through the mTOR pathway

doi: 10.16766/j.cnki.issn.1674-4152.004404
Funds:

 202103021224393

  • Received Date: 2025-09-15
    Available Online: 2026-06-02
  •   Objective  To explore the role of TRIM62 in regulating autophagy in aortic smooth muscle cells (ASMCs) and its potential mechanisms, and to evaluate its impact on vascular calcification.  Methods  Aortic smooth muscle cells were isolated and cultured from Sprague-Dawley rats. Stable cell lines were constructed for overexpression of TRIM62 (OE-TRIM62), empty vector control (Vector), knockout of TRIM62 (KO-TRIM62), and negative control (NC) groups with 12 samples in each group. Vascular calcification was induced using sodium β-glycerophosphate. Autophagy levels were assessed by monodansylcadaverine (MDC) fluorescent flow cytometry, observation of autophagosomes by transmission electron microscopy, LC3 fluorescent imaging, and adenosine triphosphate (ATP) activity assay. The expression of autophagy-related proteins (P62, ATG3, LC3) and mammalian target of rapamycin(mTOR) signaling pathway proteins (mTOR, p-mTOR) was detected by Western blot (WB).  Results  Compared with the Vector group, the median fluorescence intensity of MDC in OE-TRIM62 group was significantly increased (156.7±12.4 vs. 108.6±9.1, P < 0.05), and transmission electron microscopy showed that the number of autophagosomes increased. The ratio of p-mTOR/mTOR significantly increased (1.12±0.09 vs. 0.86±0.07, P < 0.05), and the relative expression levels of P62, ATG3, and LC3-Ⅱ proteins significantly decreased (P < 0.05). The rate of LC3 positive cells was significantly increased (24.3%±2.7% vs. 13.1%±1.8%, P < 0.05), and ATP activity was significantly decreased (P < 0.05). The p-mTOR/mTOR ratio was significantly decreased (P < 0.05), and the relative expressions of P62, ATG3 and LC3-Ⅱ proteins were significantly increased (P < 0.05). Compared with NC group, the median fluorescence intensity of MDC in KO-TRIM62 group was significantly decreased (78.4±6.2 vs. 105.3±8.7, P < 0.05). Transmission electron microscopy showed that the number of autophagosomes and the rate of LC3 positive cells were significantly decreased (6.8%±0.9% vs. 12.5%±1.6%, P < 0.05), the p-mTOR/mTOR ratio was significantly increased (P < 0.05), and the relative expressions of P62, ATG3 and LC3-Ⅱ proteins were significantly decreased (P < 0.05).  Conclusion  TRIM62 may promote the autophagy process in ASMCs by inhibiting the p-mTOR-dependent autophagy pathway, thereby relieving the suppression of autophagy by the mTOR pathway. This, in turn, may be involved in regulating the process of vascular calcification.

     

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