Loss of transcription factor ATOH8 activates TGF-β signaling and exacerbates glomerulosclerosis in podocytes

American Journal of Physiology-Renal Physiology 2026 Open access

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Authors: Hiroko Hamatani, Akifumi Tabei, Shinichiro Ogawa, Junya Suwa, Rei Ishihara, Yuki Murakami, Toru Sakairi, Hidekazu Ikeuchi, Yoriaki Kaneko, Hiroshi Handa, Masato Morikawa, Keiju Hiromura
DOI: 10.1152/ajprenal.00336.2025
Cited by: 1
References: 48

Abstract

This study identifies atonal transcription factor 8 (ATOH8) as a previously unexplored regulator of podocyte function. We demonstrate that ATOH8 knockdown activates TGF-β signaling and increases extracellular matrix gene expression. Notably, ATOH8 deficiency alone does not cause renal injury but exacerbates glomerulosclerosis in an adriamycin-induced nephropathy model, accompanied by increased Tgfb1 mRNA expression in the renal cortex. These findings indicate that ATOH8 plays a protective role in podocyte function and limits glomerulosclerosis during kidney injury.

Fields of Study & Subjects

Renal Diseases and Glomerulopathies Chronic Kidney Disease and Diabetes Genetic and Kidney Cyst Diseases

Publication details

Journal / source
American Journal of Physiology-Renal Physiology
Publisher
American Physiological Society
Volume
330
Issue
2
Pages
F269–F284
Publication date
17 January 2026
Language
EN