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TRIM36 inhibits lung fibroblast activation and pulmonary fibrosis through the degradation of phospho-AKT1

Year: 2025

Type: article

Abstract: . Mechanistically, TRIM36 mediates K48-linked polyubiquitination of phospho-AKT1 (T308/S473), leading to its proteasomal degradation and consequent inhibition of AKT signaling. Overexpression of TRIM36 markedly ameliorates bleomycin (BLM)-induced mouse pulmonary fibrosis. Taken together, these findings demonstrate that TRIM36 inhibits pulmonary fibrosis by degrading phospho-AKT1 (T308/S473) to inhibit AKT1 signaling, offering valuable insights for IPF treatment.

Source: iScience

DOI: 10.1016/j.isci.2025.113775

Authors: Yajun Li, Yuexia Yang, Yingjie Wang, Feifan Shi, Yue Zhang, Hongzhi Wen, Xin Pan, Cong Xia, Zhongzheng Li, Kaisa Cui, Guojun Zhao, Huibing Liu, Qiwen Wang, Lan Wang, Guoying Yu

Institutions: Henan Normal University, Wuxi Fourth People's Hospital, First Affiliated Hospital of Zhengzhou University

Language: English

Topic: Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis

Subfield: Pulmonary and Respiratory Medicine

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: gold

Estimated APC paid: $3,240

Funders: Ministry of Science and Technology of the People's Republic of China, China Postdoctoral Science Foundation, Key Scientific Research Project of Colleges and Universities in Henan Province, Henan Provincial Science and Technology Research Project

Awards: G1199032796, G3526413722, G3994400735, G5586842251, G6540224520, G8896032662

OpenAlex ID: W4415220847

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