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. Author manuscript; available in PMC: 2023 Dec 20.
Published in final edited form as: Circulation. 2022 Nov 24;146(25):1950–1967. doi: 10.1161/CIRCULATIONAHA.122.061960

Figure 6. Forced HMGCS2 overexpression increases adult CM dedifferentiation and proliferation for heart function improvement after myocardial infarction.

Figure 6.

A, Experimental design for performing myocardial infarction (MI) in AAV9-EGFP or AAV9-HMGCS2 mice. B, Heart function measured by echocardiography in AAV9-EGFP or AAV9-HMGCS2 mice. C, Heart function measured by catheterization in AAV9-EGFP or AAV9-HMGCS2 mice. D, The infarct area in AAV9-EGFP or AAV9-HMGCS2 hearts presented by TTC staining of heart tissues at post-MI day 21. E, Quantification of infarct percentage in AAV9-EGFP or AAV9-HMGCS2 hearts at post-MI day 21 measured by TTC staining. F, The fibrotic area in AAV9-EGFP or AAV9-HMGCS2 hearts shown by Masson Trichrome staining of heart tissue sections at post-MI day 21. G, Quantification of fibrotic percentage in AAV9-EGFP or AAV9-HMGCS2 hearts at post-MI day 21 measured by Masson Trichrome Staining. H, Immunofluorescence staining of heart tissue sections showing morphology of proliferative CMs through H3P and cTnT staining at the border zone of AAV9-EGFP or AAV9-HMGCS2 mice at post-MI day 3. Arrow heads represented H3P+/cTnT+ proliferative CMs. Scale bars were 50μm. I, Quantification of proliferative CMs (H3P+%) in the heart tissue sections of at the border zone of AAV9-EGFP or AAV9-HMGCS2 mice at post-MI day 3.