Protein acylation and heart failure: A review of novel lysine modifications in cardiac pathology

Table 1 Summary of classical lysine acetylation in pathological cardiac hypertrophy and heart failure

Typical lysine acylation	Models	Sites	Specific functions	Refs.
Acetylation	Mice	H3K4ac, H3K9ac, H3K27ac	H3K4ac, H3K9ac, and H3K27ac mediated by p300 are increased in cardiac hypertrophy and HF	[24,25]
Acetylation	Mice	H3K27ac	H3K27ac mediated by p300 exacerbates cardiac dysfunction	[26]
Acetylation	Mice	H3K9ac; H3K23ac	H3K23ac and H3K9ac are elevated in hearts of mice with diabetic cardiomyopathy	[27]
Acetylation	Mice	K3K14ac	H3K14ac is increased in mice induced by prenatal alcohol exposure, which contributed to abnormal fetal heart development	[28]
Acetylation	Rats	H3K122ac	H3K122ac is increased during the stages of HF	[29]
Acetylation	Mice, human	SERCA2a K492ac	Increased SERCA2a K492ac is associated with systolic dysfunction in HF	[30]
Acetylation	Mice	TFAM (K62ac, K76ac, K111ac, K118ac)	Acetylation of TFAM 4KR is diminished in response to low expression of GCN 5 L 1 in HF, which results in a reduction in mitochondrial DNA abundance and impaired cardiac energetics	[31]
Acetylation	Mice	P53 4KR (k98ac, K117ac, K161ac, K162ac)	Increased P53 4KR acetylation leads to coronary capillary sparsity, cardiac remodeling, and cardiac dysfunction	[32]
Acetylation	Mice	P53 K381ac	Lipopolysaccharide increases p53 K381ac and promotes the nuclear translocation of p53, contributing to cardiac dysfunction	[33]
Acetylation	Mice	Drp1 K642ac	High-fat diet leads to DRP1 K642ac increase, which activates DRP1 and results in cardiomyocyte dysfunction and death	[34]
Acetylation	Mice	SF3A2 K10ac	Ginsenoside Rb2 directly interacts with P300 to reduce SF3A2 K10ac, enhance mitochondrial respiration, and mitigate cardiac dysfunction	[35]

DRP1: Dynamin-related protein 1; HF: Heart failure; SERCA2a: Sarco/endoplasmic reticulum calcium ATPase 2a; TFAM: Mitochondrial transcription factor A.