Effects of metabolic memory on inflammation and fibrosis associated with diabetic kidney disease: an epigenetic perspective

Table 1 The administration and effect of histone PTMs regulators on DKD

Inhibitors category	Experimental models	Administration stage	Duration of treatment	Mechanisms	Ref
HAT inhibitor
Curcumin	STZ-induced SD rats	DM	4 weeks	alleviate the increase expression of ECM proteins by inhibiting HAT p300 and its binding factor NF-κB	[83]
C66	STZ-induced mice	DM	12 weeks	inhibit the increase in H3K9/14ac levels and p300/CBP occupancy on gene promoters of TCGF, PAI-1, and FN-1	[84]
HDAC inhibitor
TSA	STZ-induced SD rats	DM	4 weeks	Suppresses TGF-β1-induced epithelial-to-mesenchymal transition and activation of HDAC2	[85, 86]
Valproic acid	STZ-induced SD rats	DM	8 weeks	exert anti-inflammatory activity via reducing NF-κB and improve kidney function by reducing renal damage and fibrosis	[87]
Drugs
TSG	STZ-induced SD rats	DM	8 weeks	inhibit oxidative stress, inflammatory, and expression of TGF-β1 partly mediated by activation of SIRT1	[88]
Esculetin	STZ-induced SD rats	DKD	8 weeks	attenuate alteration in Mmp13 and Bmp6 gene expression by involving change in acetylation and methylation of histone H3	[89]

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