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Review Article | Open Access

Role of autophagy and histone deacetylases in diabetic nephropathy: Current status and future perspectives

Sabbir KhanZahid Rafiq BhatGopabandhu Jena,( )
Facility for Risk Assessment and Intervention Studies, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Sector-67, S.A.S. Nagar, Punjab, 160062, India

Peer review under responsibility of Chongqing Medical University.

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Abstract

The prevalence of diabetes and its complications is increasing at an alarming rate in both developed and deve1oping nations. The emerging evidences highlighted that both genetic and epigenetic mechanisms including histone modifications play a significant role in the pathogenesis of diabetic nephropathy (DN). Histone deacetylases (HDACs) and acetylation are involved in the regulation of autophagy as well as pathogenesis of DN. Both HDACs and histone acetyltransferases (HATs) play a key role in chromatin remodeling and affect the transcription of various genes involved in the cellular homeostasis, apoptosis, immunity and angiogenesis. Further, HDAC inhibitors are exert the renoprotective effects in DN and other diabetic complications. Thus, the cellular acetylation plays a crucial role in the regulation of autophagy and can be explored as a new therapeutic target for the treatment of DN. This review aimed to delineate the role of HDACs and associated molecular signaling/pathways in the regulation of autophagy with an emphasis on promising targets for the treatment of DN.

Genes & Diseases
Pages 211-219
Cite this article:
Khan S, Bhat ZR, Jena G. Role of autophagy and histone deacetylases in diabetic nephropathy: Current status and future perspectives. Genes & Diseases, 2016, 3(3): 211-219. https://doi.org/10.1016/j.gendis.2016.04.003

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Received: 21 January 2016
Accepted: 16 April 2016
Published: 23 April 2016
© 2016 Chongqing Medical University.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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