Epigenetic regulation and post-translational modifications of ferroptosis-related factors in cardiovascular diseases

Table 3 Ferroptosis-regulating methylation in CVDs

Modification	Diseases	Targets	Biological functions	References
Methylation	DIC	Nrf2/GPX4	PRMT4 interacts with Nrf2 to limit the nuclear translocation of Nrf2 and suppressing the transcription of GPX4	[82]
Methylation	DdCM	NCOA4	Inhibition of DNMT-1 could reduce ferroptosis by participation of NCOA4-mediated ferritinophagy	[82]
m6A	AD	SLC7A11	METTL3 was significantly upregulated in the aorta of patients with thoracic aortic aneurysm and dissection, it can promote ferroptosis by inhibiting the expression of SLC7A11 and FPS1	[86]
m6A	DIC	TFR	Doxorubicin led to upregulation of METTL14, catalyzed the m6A modification of the lncRNA KCNQ1OT1, which led to increased levels of TFR1, thereby increasing ferroptosis in DIC	[87]
m6A	DIC	P53	FTO mediates m6A demethylation of P53 or P21/Nrf2 in a human antigen R-dependent manner, inhibiting doxorubicin-induced ferroptosis through the activation of P21/Nrf2	[88]
m6A	Sepsis‑induced myocardial	SLC7A11	METTL3-mediated methylation of SLC7A11 could result in YTHDF2 mediated mRNA degradation of SLC7A11.thereby upregulating ferroptosis in sepsis-induced myocardial injury	[89]

DIC: doxorubicin-induced cardiomyopathy, AD: aortic aneurysm and dissection, PRMT4: protein arginine methyltransferase 4, FSP1: ferroptosis suppressor protein 1, FTO: fat mass and obesity-associated protein, YTHDF2: YTH N6-methyladenosine RNA-binding protein F2

ISSN: 1868-7083