Inhibition of Fibrogenesis upon Hydralazine-induced DNA Demethylation

Abstract

Chronic progressive kidney disease (CKD) remains an unsolved problem in clinical Nephrology as neither biomarkers to predict progression towards end-stage renal failure in individual patients nor specific drugs to inhibit decline of kidney function are available in the clinic yet. In this regard, the prototypical epigenetic mechanism of CpG island promoter methylation has emerged as modulator of disease progression with utilities both as biomarker and as therapeutic target. Recent studies demonstrated the potential of hydralazine, a long-established antihypertensive drug with de-methylating activity, to reverse aberrant CpG island promoter aberration and ameliorate progression of chronic kidney disease. Here we review contribution of aberrant promoter methylation to progression of fibrogenesis and mechanisms underlying hydralazine's demethylating activity and discuss possible translational implications.Citation: Zeisberg EM, Zeisberg M (2016) Inhibition of Fibrogenesis upon Hydralazine-induced DNA Demethylation. J Kidney 2: 124.