HDAC4 blocks autophagy to trigger podocyte injury: Non-epigenetic action in diabetic nephropathy

Research output: Contribution to journalComment/debate

20 Scopus citations


Histone deacetylases (HDACs) have been implicated in the pathogenesis of kidney diseases including diabetic nephropathy (DN); however, the mechanism is poorly understood. Wang et al. unravel the changes in expression of various HDACs in DN and demonstrate that HDAC4 specifically contributes to podocyte injury in DN. HDAC4 deacetylates STAT1 to suppress autophagy, an essential cellular process for the function and viability of podocytes. The development of HDAC isoform-specific inhibitors may provide efficacious therapeutics for DN and related renal diseases.

Original languageEnglish (US)
Pages (from-to)666-668
Number of pages3
JournalKidney International
Issue number4
Publication statusPublished - Jan 1 2014


ASJC Scopus subject areas

  • Nephrology

Cite this