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10.1038/ki.2014.142

http://scihub22266oqcxt.onion/10.1038/ki.2014.142
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C4181378!4181378!25265947
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suck abstract from ncbi


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pmid25265947      Kidney+Int 2014 ; 86 (4): 666-8
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  • HDAC4 blocks autophagy to trigger podocyte injury: non-epigenetic action in diabetic nephropathy #MMPMID25265947
  • Wei Q; Dong Z
  • Kidney Int 2014[Oct]; 86 (4): 666-8 PMID25265947show ga
  • Histone deacetylases (HDACs) have been implicated in the pathogenesis of kidney diseases including diabetic nephropathy (DN); however, the underlying mechanism is poorly understood. In this issue, Wang et. al. have unraveled the changes in expression of various HDACs in DN and demonstrated that HDAC4 specifically contributes to podocyte injury in this disease. Mechanistically, 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.
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