HDAC4 blocks autophagy to trigger podocyte injury: non-epigenetic action in diabetic nephropathy.
Where this comes from
- Record sourced from PubMed, PMID 25265947.
- Also identified by DOI 10.1038/ki.2014.142 and PMC identifier 4181378.
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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.
Medical subject headings
- Diabetic Nephropathies
- Histone Deacetylases
- Podocytes
- Repressor Proteins