title: HDAC4 blocks autophagy to trigger podocyte injury: non-epigenetic action in diabetic nephropathy.
abstract: 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.
authors.affiliation: Department of Cellular Biology and Anatomy, Medical College of Georgia, Georgia Regents University and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia, USA.
authors.forename: Qingqing
authors.initials: Q
authors.lastname: Wei
authors.affiliation: 1] Department of Cellular Biology and Anatomy, Medical College of Georgia, Georgia Regents University and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia, USA [2] Department of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
authors.forename: Zheng
authors.initials: Z
authors.lastname: Dong
mesh_terms: D000818:Animals; D003928:Diabetic Nephropathies / Q000378:metabolism* / Q000473:pathology*; D006655:Histone Deacetylases / Q000378:metabolism*; D006801:Humans; D008297:Male; D050199:Podocytes / Q000378:metabolism* / Q000473:pathology*; D012097:Repressor Proteins / Q000378:metabolism*
chemical_list: D012097:Repressor Proteins; D006655:Histone Deacetylases