Role of Epigenetic Histone Modifications in Diabetic Kidney Disease Involving Renal Fibrosis

Table 1

Effects of HDAC inhibitors on diabetic kidney disease.

HDAC inhibitors	Selectivity	Experimental model	Effects	Mechanism	References
Valproic acid	HDAC I/II	STZ-induced diabetic rat kidneys and; TGF-β1-treated NRK52-E cells	Decreases ECM components and prevents EMT	Suppresses TGF-β1-induced; activation of HDAC-2	[77]
		STZ-induced diabetic kidneys	Alleviates the renal damage and fibrosis	Repressing the myofibroblast; transformation and fibrogenesis	[83]
TSA	HDAC I/II	STZ-induced diabetic rat kidneys and; TGF-β1-treated NRK52-E cells	Decreases ECM components and prevents EMT	Suppresses TGF-β1-induced; activation of HDAC-2	[77]
		TGF-β1-treated RMCs	Further increased TGF-β1-stimulated PAI-1; gene transcriptional capability and expression	Further amplified TGF-β1-motivated H3K9/14Ac levels	[62]
SK7041	HDAC I	STZ-induced diabetic rat kidneys and; TGF-β1-treated NRK52-E cells	Decreases ECM components and prevents EMT	Suppresses TGF-β1-induced; activation of HDAC-2	[77]
Vorinostat	HDAC I/II	Cultured proximal tubule cells and STZ-induced diabetic kidneys	Attenuated cellular proliferation, suppressed glomerular hypertrophy	Downregulated EGFR expression	[85]
		STZ-diabetic mice	Decreased oxidative stress, albuminuria, and collagen IV deposition	Interplay between eNOS activity and oxidative stress	[86]
Sodium butyrate (NaB)	Pan HDAC inhibitor	STZ-induced diabetic kidneys	Ameliorated renal function and relieved histological; alterations, apoptosis, fibrosis, and DNA damage	NA	[87]