Fig. 4: Increased monocyte infiltration mediated by CLYBL hyperacetylation aggravates cardiac remodeling. | Cell Death & Disease

Fig. 4: Increased monocyte infiltration mediated by CLYBL hyperacetylation aggravates cardiac remodeling.

From: Positive feedback loop involving AMPK and CLYBL acetylation links metabolic rewiring and inflammatory responses

Fig. 4

A Hearts from SIRT2-WT and SIRT2-KO mice injected with saline or Ang II (1.4 mg/kg/d) for 4 weeks were used to detect the acetylation of CLYBL (*p < 0.05; **p < 0.01). B H&E (upper), Scale bar, 2 mm; WGA (centered), Scale bar, 20 μm; and Masson’s trichrome staining (lower), Scale bar, 20 μm. C Measurements of representative heart specimens. D Echocardiogram was used to assess cardiac function. E, F Ejection fraction and fractional shortening in WT and SIRT2-KO mice treated with saline or Ang II (**p < 0.01; ***p < 0.001). G Expression levels of myocardial injury markers (ANP, BNP) were evaluated using western blotting (*p < 0.05; **p < 0.01; ***p < 0.001). H Immunofluorescence was used to detect CD68 (CD68 red, DAPI blue; Scale bar, 100 μm). I qPCR was used to assess the relative levels of IL-6 and IL-1β (*p < 0.05; **p < 0.01).

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