©The Author(s) 2025.
World J Diabetes. Dec 15, 2025; 16(12): 112423
Published online Dec 15, 2025. doi: 10.4239/wjd.v16.i12.112423
Published online Dec 15, 2025. doi: 10.4239/wjd.v16.i12.112423
Figure 7 The molecular mechanism of the improvement of liraglutide in diabetic cardiomyopathy.
Graphic summary demonstrating liraglutide could be a novel AMPK-Parkin activator to ameliorate myocardial dysfunction in high-fat diet and streptozotocin induced rat. In diabetes, liraglutide increases phosphorylation of AMPK, upregulates the expression of PTEN-induced putative kinase 1 and Parkin, and then, recruits and phosphorylates more Parkin, activates mitophagy, and improves mitochondrial function (mitochondrial membrane potential recovery, mitochondrial reactive oxygen species level decrease and ATP content increase). HFD: High-fat diet; STZ: Streptozotocin; HG: High glucose; PA: Palmitic acid; ∆Ψm: Mitochondrial membrane potential. Created in BioRender (Supplementary material).
- Citation: Zhu YX, Zhang W, Qu HL, Zhang Y, Zhou RQ, Li P, Wang F, Zhang Y, Liu HH, Li S, Dong Q, Dou KF, Guo YL, Li JJ, Xu RX. Liraglutide alleviates diabetic cardiomyopathy in streptozotocin-induced diabetic rats by enhancing mitophagy mediated by the AMPK-Parkin signaling pathway. World J Diabetes 2025; 16(12): 112423
- URL: https://www.wjgnet.com/1948-9358/full/v16/i12/112423.htm
- DOI: https://dx.doi.org/10.4239/wjd.v16.i12.112423