Fig. 3: HMGA1 overexpression accelerates cardiac remodeling in DCM mouse hearts. | Cell Death & Disease

Fig. 3: HMGA1 overexpression accelerates cardiac remodeling in DCM mouse hearts.

From: High-mobility group AT-hook 1 promotes cardiac dysfunction in diabetic cardiomyopathy via autophagy inhibition

Fig. 3

a, c–g Mice received an AAV9-HMGA1 injection at 10 weeks after the final STZ injection (n = 12 per group). a Protein levels of HMGA1 in mouse hearts 6 weeks after AAV9-HMGA1 injection and with or without STZ injection (n = 6 mice hearts). b Mice received an AAV9-HMGA1 injection for 6 weeks. The expression of HMGA1 in cardiomyocytes (n = 6) and fibroblasts (n = 6) isolated from heart tissues. c Body weights and blood glucose levels in DCM mice 0, 1, 2, 3, and 4 months after the final STZ injection (n = 12 sample). d Immunohistochemical staining and quantification results for CD45, CD68, and TNFα in DCM mouse hearts (n = 5). e mRNA levels of proinflammatory markers in DCM mouse hearts (n = 6). f TUNEL staining and quantification results in DCM mouse hearts (n = 5). g Protein levels of Bax, Bcl-2, and cytochrome C in DCM mouse hearts (n = 6). *P < 0.05 vs. the AAV9-NC-CON group; #P < 0.05 vs. the AAV9-NC-DCM group.

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