fig 2 (IMAGE)
Caption
Fig 2: The schematic illustrating that long-term EGCG administration prevents CDD and cTnI decline in aging hearts. The scheme depicts the role of physiological aging in the pathophysiology of CDD. The hallmarks of HFpEF such as CDD, reduced exercise performance, increased heart failure markers, myocardial fibrosis, cardiomyocyte apoptosis, and mitochondrial destruction, which might be associated with cTnI decline induced by HDAC1. According to our results, long-term EGCG administration counteracts aging-associated cardiomyocyte apoptosis and mitochondrial destruction, through which it improves the physiological cardiac function and structure. In the aging mice, EGCG regulates cTnI gene expression via inhibiting the expression of HDAC1, reducing its binding level near cTnI's promoter region and lowering the activity, as well as enhancing AcH3 and AcH3K9. The black blue arrow indicates lower and the red arrow indicates higher. See text for details. AcH3, acetylated histone 3; AcH3K9, acetylated lysine 9 on histone H3; CDD, cardiac diastolic dysfunction; cTnI, cardiac troponin I; EGCG, epigallocatechin gallate; HDAC1, histone deacetylase 1; HFpEF, heart failure with preserved ejection fraction.
Credit
Genes & Diseases
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