Metabolic derangement in polycystic kidney disease mouse models is ameliorated by mitochondrial-targeted antioxidants

Nastaran Daneshgar; Andrew W. Baguley; Peir-In Liang; Fei Wu; Yi Chu; Michael T. Kinter; Gloria A. Benavides; Michelle S. Johnson; Victor Darley-Usmar; Jianhua Zhang; Kung-Sik Chan; Dao-Fu Dai

doi:10.1038/s42003-021-02730-w

Communications Biology (Oct 2021)

Metabolic derangement in polycystic kidney disease mouse models is ameliorated by mitochondrial-targeted antioxidants

Nastaran Daneshgar,
Andrew W. Baguley,
Peir-In Liang,
Fei Wu,
Yi Chu,
Michael T. Kinter,
Gloria A. Benavides,
Michelle S. Johnson,
Victor Darley-Usmar,
Jianhua Zhang,
Kung-Sik Chan,
Dao-Fu Dai

Affiliations

Nastaran Daneshgar: Department of Pathology, Carver College of Medicine, University of Iowa
Andrew W. Baguley: Department of Pathology, Carver College of Medicine, University of Iowa
Peir-In Liang: Department of Pathology, Carver College of Medicine, University of Iowa
Fei Wu: Department of Statistics and Actuarial Science, College of Liberal Arts and Sciences, University of Iowa
Yi Chu: Department of Pathology, Carver College of Medicine, University of Iowa
Michael T. Kinter: Aging & Metabolism Research Program, Oklahoma Medical Research Foundation
Gloria A. Benavides: Department of Pathology, Mitochondrial Medicine Laboratory, University of Alabama
Michelle S. Johnson: Department of Pathology, Mitochondrial Medicine Laboratory, University of Alabama
Victor Darley-Usmar: Department of Pathology, Mitochondrial Medicine Laboratory, University of Alabama
Jianhua Zhang: Department of Pathology, Mitochondrial Medicine Laboratory, University of Alabama
Kung-Sik Chan: Department of Statistics and Actuarial Science, College of Liberal Arts and Sciences, University of Iowa
Dao-Fu Dai: Department of Pathology, Carver College of Medicine, University of Iowa

DOI: https://doi.org/10.1038/s42003-021-02730-w
Journal volume & issue: Vol. 4, no. 1
pp. 1 – 13

Abstract

Read online

Daneshgar et al. investigated the role of mitochondrial dysfunction in ADPKD and mitochondria protective agents as potential therapeutics. The authors reported decreased mitochondrial complex activity and downregulation of mitochondrial and metabolic proteins in ADPKD, and proposed mCAT overexpression or SS31 treatment to slow cystogenesis.

Published in Communications Biology

ISSN: 2399-3642 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science: Biology (General)
Website: https://www.nature.com/commsbio/

About the journal