HIF-1 contributes to autophagy activation via BNIP3 to facilitate renal fibrosis in hypoxia in vitro and UUO in vivo

Author:

Liu Jing12,Livingston Man J.2ORCID,Dong Guie2,Wei Qingqing2ORCID,Zhang Ming2,Mei Shuqin23,Zhu Jiefu4,Zhang Chun1ORCID,Dong Zheng2ORCID

Affiliation:

1. Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

2. Department of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University and Charlie Norwood VA Medical Center, Augusta, Georgia, United States

3. Department of Nephrology, Second Affiliated Hospital of Naval Medical University, Shanghai, China

4. Department of Urology, Renmin Hospital of Wuhan University, Wuhan, China

Abstract

Autophagy has been reported to participate in renal fibrosis, but its role and underlying activation mechanism is unclear. In this study, we report the role of HIF-1 in autophagy activation in models of renal fibrosis and further investigate the underlying mechanism.

Funder

HHS | National Institutes of Health

U.S. Department of Veterans Affairs

National Natural Science Foundation of China

湖北省科技厅 | Natural Science Foundation of Hubei Province

Publisher

American Physiological Society

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