NDUFS4 regulates cristae remodeling in diabetic kidney disease

Koki Mise, Jianyin Long, Daniel L. Galvan, Zengchun Ye, Guizhen Fan, Rajesh Sharma, Irina I. Serysheva, Travis I. Moore, Collene R. Jeter, M. Anna Zal, Motoo Araki, Jun Wada, Paul T. Schumacker, Benny H. Chang and Farhad R. Danesh ()
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Koki Mise: The University of Texas MD Anderson Cancer Center
Jianyin Long: The University of Texas MD Anderson Cancer Center
Daniel L. Galvan: The University of Texas MD Anderson Cancer Center
Zengchun Ye: The Third Affiliated Hospital of Sun Yat-Sen University
Guizhen Fan: The University of Texas Health Science Center at Houston
Rajesh Sharma: The University of Texas Health Science Center at Houston
Irina I. Serysheva: The University of Texas Health Science Center at Houston
Travis I. Moore: The University of Texas Health Science Center at Houston
Collene R. Jeter: The University of Texas MD Anderson Cancer Center
M. Anna Zal: The University of Texas MD Anderson Cancer Center
Motoo Araki: Okayama University Graduate School of Medicine, Dentistry & Pharmaceutical Sciences
Jun Wada: Rheumatology, Endocrinology & Metabolism, Okayama University Graduate School of Medicine, Dentistry & Pharmaceutical Sciences
Paul T. Schumacker: Feinberg School of Medicine, Northwestern University
Benny H. Chang: The University of Texas MD Anderson Cancer Center
Farhad R. Danesh: The University of Texas MD Anderson Cancer Center

Nature Communications, 2024, vol. 15, issue 1, 1-19

Abstract: Abstract The mitochondrial electron transport chain (ETC) is a highly adaptive process to meet metabolic demands of the cell, and its dysregulation has been associated with diverse clinical pathologies. However, the role and nature of impaired ETC in kidney diseases remains poorly understood. Here, we generate diabetic mice with podocyte-specific overexpression of Ndufs4, an accessory subunit of mitochondrial complex I, as a model investigate the role of ETC integrity in diabetic kidney disease (DKD). We find that conditional male mice with genetic overexpression of Ndufs4 exhibit significant improvements in cristae morphology, mitochondrial dynamics, and albuminuria. By coupling proximity labeling with super-resolution imaging, we also identify the role of cristae shaping protein STOML2 in linking NDUFS4 with improved cristae morphology. Together, we provide the evidence on the central role of NDUFS4 as a regulator of cristae remodeling and mitochondrial function in kidney podocytes. We propose that targeting NDUFS4 represents a promising approach to slow the progression of DKD.

Date: 2024
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DOI: 10.1038/s41467-024-46366-w

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