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

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 HDAC...

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Detalles Bibliográficos
Autores principales: Wei, Qingqing, Dong, Zheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2014
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4181378/
https://www.ncbi.nlm.nih.gov/pubmed/25265947
http://dx.doi.org/10.1038/ki.2014.142
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author Wei, Qingqing
Dong, Zheng
author_facet Wei, Qingqing
Dong, Zheng
author_sort Wei, Qingqing
collection PubMed
description 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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spelling pubmed-41813782015-04-01 HDAC4 blocks autophagy to trigger podocyte injury: non-epigenetic action in diabetic nephropathy Wei, Qingqing Dong, Zheng Kidney Int Article 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. 2014-10 /pmc/articles/PMC4181378/ /pubmed/25265947 http://dx.doi.org/10.1038/ki.2014.142 Text en http://www.nature.com/authors/editorial_policies/license.html#terms Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms
spellingShingle Article
Wei, Qingqing
Dong, Zheng
HDAC4 blocks autophagy to trigger podocyte injury: non-epigenetic action in diabetic nephropathy
title HDAC4 blocks autophagy to trigger podocyte injury: non-epigenetic action in diabetic nephropathy
title_full HDAC4 blocks autophagy to trigger podocyte injury: non-epigenetic action in diabetic nephropathy
title_fullStr HDAC4 blocks autophagy to trigger podocyte injury: non-epigenetic action in diabetic nephropathy
title_full_unstemmed HDAC4 blocks autophagy to trigger podocyte injury: non-epigenetic action in diabetic nephropathy
title_short HDAC4 blocks autophagy to trigger podocyte injury: non-epigenetic action in diabetic nephropathy
title_sort hdac4 blocks autophagy to trigger podocyte injury: non-epigenetic action in diabetic nephropathy
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4181378/
https://www.ncbi.nlm.nih.gov/pubmed/25265947
http://dx.doi.org/10.1038/ki.2014.142
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