©The Author(s) 2026.
World J Diabetes. Jan 15, 2026; 17(1): 112027
Published online Jan 15, 2026. doi: 10.4239/wjd.v17.i1.112027
Published online Jan 15, 2026. doi: 10.4239/wjd.v17.i1.112027
Figure 6 Impact of UNC-51-like kinase 1 upregulation on the mitophagy-associated proteins and the mitochondrial membrane potential in diabetic cardiomyopathy.
A and B: UNC-51-like kinase 1 protein levels in diabetic cardiomyopathy (DCM) mice; C-G: Western blotting quantification of Beclin1, p62, Parkin, and microtubule-associated protein 1 light chain 3B proteins in DCM mice; H-M: Western blotting quantification of mitophagy-associated proteins (UNC-51-like kinase 1, p62, Parkin, Beclin1, and microtubule-associated protein 1 light chain 3B) in DCM cell models; N: Electron micrographs of mitophagy (scale bar: 2 μm); O: Changes in the mitochondrial membrane potential (scale bar: 50 μm); P: Statistical analysis of mitophagy from electron micrographs; Q: Statistical analysis of the mitochondrial membrane potential. Values are mean ± SD (n = 4). aP < 0.05, and bP < 0.01. Con: Control; DCM: Diabetic cardiomyopathy; ULK1: UNC-51-like kinase 1; GAPDH: Glyceraldehyde 3-phosphate dehydrogenase; OE: Overexpress; NC: Negative control; LC3B: Microtubule-associated protein 1 light chain 3B; HG: High glucose; EV: Empty vector; EM: Electron microscopy.
- Citation: Wu Y, Wang WY, Zhang JQ, Wang S, Zeng Z, Fu L, Li B. Microtubule affinity-regulating kinase 4 exacerbates diabetic cardiomyopathy by inhibiting UNC-51-like kinase 1-mediated mitochondrial autophagy. World J Diabetes 2026; 17(1): 112027
- URL: https://www.wjgnet.com/1948-9358/full/v17/i1/112027.htm
- DOI: https://dx.doi.org/10.4239/wjd.v17.i1.112027