STAT3 inhibition attenuates the progressive phenotypes of Alport syndrome mouse model | Zendy

Tsubasa Yokota | Zendy; Kohei Omachi | Zendy; Mary Ann Suico | Zendy; Misato Kamura | Zendy; Haruka Kojima | Zendy; Ryosuke Fukuda | Zendy; Keishi Motomura | Zendy; Keisuke Teramoto | Zendy; Shota Kaseda | Zendy; Jun Kuwazuru | Zendy; Toru Takeo | Zendy; Naomi Nakagata | Zendy; Tsuyoshi Shuto | Zendy; Hirofumi Kai | Zendy

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STAT3 inhibition attenuates the progressive phenotypes of Alport syndrome mouse model

Author(s) -

Tsubasa Yokota,

Kohei Omachi,

Mary Ann Suico,

Misato Kamura,

Haruka Kojima,

Ryosuke Fukuda,

Keishi Motomura,

Keisuke Teramoto,

Shota Kaseda,

Jun Kuwazuru,

Toru Takeo,

Naomi Nakagata,

Tsuyoshi Shuto,

Hirofumi Kai

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/gfx246

Subject(s) - medicine , alport syndrome , stat3 , blood urea nitrogen , glomerulosclerosis , creatinine , fibrosis , endocrinology , kidney , nephritis , renal function , proteinuria , cancer research , signal transduction , glomerulonephritis , biology , microbiology and biotechnology

Alport syndrome (AS) is a hereditary, progressive nephritis caused by mutation of type IV collagen. Previous studies have shown that activation of signal transducer and activator of transcription 3 (STAT3) exacerbates other renal diseases, but whether STAT3 activation exacerbates AS pathology is still unknown. Here we aim to investigate the involvement of STAT3 in the progression of AS.

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