Histone Acetylation and Its Modifiers in the Pathogenesis of Diabetic Nephropathy

Table 2

Reported HATs/HDACs in DN.

Enzyme category	Enzymes	Catalyzed site	Target renal loci	Effects in DN	References
HATs	CBP	H3K9/14, H4K5/8/12	Human monocytes; RMCs	Inflammation; increased TGF-β1-induced genes expression	[30, 36]
	GCN5		Akita mice renal cortex	Inflammation	[33]
	P300	H3K9/14	Endothelial cell, diabetic rats; RMCs	Inflammation, FN, vasoactive factors; increased TGF-β1-induced genes expression	[36, 54, 56]
	p/CAF	H3K9/14, H4K5/8/12; H3K18	Human monocytes; Akita mice renal cortex; db/db mice, human renal proximal tubule epithelial cell line	Inflammation	[30, 57]
HDACs	HDAC1	H3K9/14; H3K9, H3K18	RMCs; Akita mice, HBZY-1 cell	Blocking TGF-β1-induced gene expression; affecting inflammatory factors	[33, 36]
	HDAC2	H3/H4	Type1/2 murine models, NRK52-E cells	Promoting fibrosis	[68]
	HDAC4		Db/db mice, STZ-induced rats, diabetic patients	Contributing to podocyte injury	[70]
	HDAC5	H3K9/14	RMCs	Blocking TGF-β1-induced gene expression	[36]
	SIRT1	NF-κB, STAT3	Renal tubular cells, podocyte; GMCs; db/db mice; diabetic fa/fa rats	Attenuating albuminuria; inhibiting cell apoptosis; attenuating kidney injury; regulating autophagy; reducing oxidative stress	[47, 75–80, 82–84]