Open AccessmiR-29b attenuates histone deacetylase-4 mediated podocyte dysfunction and renal fibrosis in diabetic nephropathy
Author(s) -
Piyush Gondaliya,
Aishwarya Dasare,
Kavya Jash,
Rakesh Kumar Tekade,
Akshay Srivastava,
Kiran Kalia
Publication year - 2019
Publication title -
journal of diabetes and metabolic disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.619
H-Index - 33
ISSN - 2251-6581
DOI - 10.1007/s40200-019-00469-0
Subject(s) - hdac4 , podocyte , medicine , diabetic nephropathy , histone deacetylase , cancer research , downregulation and upregulation , fibrosis , inflammation , histone , microbiology and biotechnology , endocrinology , kidney , biology , proteinuria , biochemistry , gene
As epigenetic modifications like chromatin histone modifications have been suggested to play a role in the pathophysiology of Diabetic Nephropathy (DN) and are also found to be regulated by microRNAs. Our main purpose was to explore the role of microRNA in histone modulations associated with DN. There is downregulation of miR-29b due to advanced glycation end products in diabetes. Histone Deacetylase-4 (HDAC4) is amongst the histone modulators which promotes podocytes' impairment and upregulates transforming growth factor-1 (TGF-β1) leading to renal fibrosis. Moreover, macrophage infiltration causes podocytes' apoptosis and IL-6 mediated inflammation. As miR-29b is downregulated in diabetes and HDAC4, TGF-β1 and IL-6 could be the possible therapeutic targets in DN, our study was focussed on unveiling the role of miR-29b in modulation of HDAC4 and hence, in podocyte dysfunction and renal fibrosis in DN.