Repression of hypoxia-inducible factor-1 contributes to increased mitochondrial reactive oxygen species production in diabetes

• Published in: eLife Vol. 11
• Main Authors: Zheng, Xiaowei, Narayanan, Sampath, Xu, Cheng, Eliasson Angelstig, Sofie, Grünler, Jacob, Zhao, Allan, Di Toro, Alessandro, Bernardi, Luciano, Mazzone, Massimiliano, Carmeliet, Peter, Del Sole, Marianna, Solaini, Giancarlo, Forsberg, Elisabete A, Zhang, Ao, Brismar, Kerstin, Schiffer, Tomas A, Rajamand Ekberg, Neda, Botusan, Ileana Ruxandra, Palm, Fredrik, Catrina, Sergiu-Bogdan
• Format: Journal Article
• Language: English
• Published: England eLife Science Publications, Ltd 15.02.2022; eLife Sciences Publications Ltd; eLife Sciences Publications, Ltd
• Subjects: Adult; Analysis; Animal models; Animals; Apoptosis; Cell Biology; Cell culture; Cell Line; Dextrose; Diabetes; Diabetes Complications; Diabetes mellitus (insulin dependent); Diabetes Mellitus - blood; Diabetes Mellitus - genetics; diabetic complications; Female; Glucose; Glycerol; Health aspects; Human; Humans; Hydroxylase; Hyperglycemia; Hyperglycemia - genetics; Hypoxia; Hypoxia-inducible factor 1; Hypoxia-Inducible Factor 1 - antagonists & inhibitors; Hypoxia-Inducible Factor 1 - genetics; Kidney - pathology; Kidneys; Male; Medicine; Mice; Mitochondria; Mitochondria - metabolism; Mouse; Plasmids; Pyruvic acid; Reactive oxygen species; Reactive Oxygen Species - blood; Reactive Oxygen Species - metabolism; Signal Transduction; Spectrum analysis; Therapeutic targets; Transcription factors; Type 1 diabetes; Young Adult; Canada; United States > US; diabetic complications; hypoxia; mouse; cell biology; mitochondria; hypoxia-inducible factor-1; reactive oxygen species; medicine; diabetes; human

Excessive production of mitochondrial reactive oxygen species (ROS) is a central mechanism for the development of diabetes complications. Recently, hypoxia has been identified to play an additional pathogenic role in diabetes. In this study, we hypothesized that ROS overproduction was secondary to t...