Mitophagy in Diabetic Kidney Disease

Diabetic kidney disease (DKD) is the most common cause of end-stage kidney disease worldwide and is the main microvascular complication of diabetes. The increasing prevalence of diabetes has increased the need for effective treatment of DKD and identification of new therapeutic targets for better cl...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in cell and developmental biology Vol. 9; p. 778011
Main Authors Zhang, Xiaofeng, Feng, Jing, Li, Xia, Wu, Dan, Wang, Qian, Li, Shuyu, Shi, Changhua
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 10.12.2021
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Diabetic kidney disease (DKD) is the most common cause of end-stage kidney disease worldwide and is the main microvascular complication of diabetes. The increasing prevalence of diabetes has increased the need for effective treatment of DKD and identification of new therapeutic targets for better clinical management. Mitophagy is a highly conserved process that selectively removes damaged or unnecessary mitochondria the autophagic machinery. Given the important role of mitophagy in the increased risk of DKD, especially with the recent surge in COVID-19-associated diabetic complications, in this review, we provide compelling evidence for maintaining homeostasis in the glomeruli and tubules and its underlying mechanisms, and offer new insights into potential therapeutic approaches for treatment of DKD.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
Edited by: Gong-Ping Liu, Huazhong University of Science and Technology, China
Ivana Novak, School of Medicine, Croatia
Reviewed by: Jun Ren, University of Washington, United States
These authors have contributed equally to this work
This article was submitted to Molecular and Cellular Pathology, a section of the journal Frontiers in Cell and Developmental Biology
ISSN:2296-634X
2296-634X
DOI:10.3389/fcell.2021.778011