Heterozygosity of mitogen-activated protein kinase organizer 1 ameliorates diabetic nephropathy and suppresses epithelial-to-mesenchymal transition-like changes in db/db mice | Zendy

Ivonne Loeffler | Zendy; Marita Liebisch | Zendy; Christoph Daniel | Zendy; Kerstin Amann | Zendy; Günter Wolf | Zendy

Open Access

Heterozygosity of mitogen-activated protein kinase organizer 1 ameliorates diabetic nephropathy and suppresses epithelial-to-mesenchymal transition-like changes in db/db mice

Author(s) -

Ivonne Loeffler,

Marita Liebisch,

Christoph Daniel,

Kerstin Amann,

Günter Wolf

Publication year - 2017

Publication title -

nephrology dialysis transplantation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.654

H-Index - 168

eISSN - 1460-2385

pISSN - 0931-0509

DOI - 10.1093/ndt/gfx202

Subject(s) - diabetic nephropathy , medicine , endocrinology , fibrosis , kidney , epithelial–mesenchymal transition , protein kinase a , nephropathy , kidney disease , mapk/erk pathway , genetically modified mouse , diabetes mellitus , kinase , cancer research , transgene , biology , microbiology and biotechnology , gene , biochemistry , cancer , metastasis

Progressive diabetic nephropathy (DN) is characterized by tubulointerstitial fibrosis that is caused by accumulation of extracellular matrix. Induced by several factors, matrix-producing myofibroblasts may to some extent originate from tubular cells by epithelial-to-mesenchymal transition (EMT). Although previous data document that activation of hypoxia-inducible factor (HIF) signalling can be renoprotective in acute kidney disease, this issue remains controversial in chronic kidney injury. Here, we studied whether DN and EMT-like changes are ameliorated in a mouse model of type 2 diabetes mellitus with increased stability and activity of the HIF.

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