Topical Collection "Mitochondrial Dysfunction in Kidney Diseases"

A topical collection in Cells (ISSN 2073-4409). This collection belongs to the section "Autophagy".

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Division of Nephrology and Hypertension, Joan and Sanford I. Weill Department of Medicine, NewYork-Presbyterian Hospital, Weill Cornell Medicine, New York, NY, USA
Interests: mitophagy; mitochondrial dysfunction; autophagy; immune cells; macrophages; kidney diseases; kidney fibrosis

Topical Collection Information

Dear Colleagues,

Mitochondria satisfy the high metabolic needs of the kidney and efficiently combat kidney injury-induced stresses. The kidney has the highest number of mitochondria after the heart. Mitochondrial structural and functional aberrations are widely reported during both acute kidney injury (AKI) and chronic kidney disease (CKD). Mitochondrial dysfunction is an early event during kidney injury, and exerts a critical role in exaggerating inflammation in various forms of AKI, including cisplatin, sepsis, or ischemia-reperfusion-mediated kidney injuries. Defects in mitochondrial quality control and bioenergetics are also known to promote inflammatory and fibrotic responses and progression of tubulointerstitial fibrosis in different forms of CKD, including diabetic, membranous, and IgA nephropathies and polycystic kidney disease.

Both the production of new mitochondrial networks and recycling of dysfunctional mitochondria via mitophagy in the kidney are crucial, and help maintain the overall metabolic status, sensing and responding to different triggers and oxidative stress. The balance between mitochondrial fusion and fission processes also influences mitochondrial structure and functions. Hyperfused mitochondria produce higher energy, while fragmented mitochondria with impaired membrane potentials are recycled through mitophagy. The therapeutic approaches that help in regulating mitochondrial health have the potential to attenuate cell death related to kidney injury-induced inflammation, tissue disruption, failure of tissue repair, and resultant tubulointerstitial fibrosis and progression of CKD to end-stage kidney disease.

In this Special Issue, we invite submissions focused on investigating mitochondrial functions, associated molecular pathways including mitophagy, approaches to study mitochondrial dynamics (fusion/fission) during AKI and CKD using different experimental models of kidney diseases, and mitochondria-targeted potential therapeutic strategies.

Dr. Divya Bhatia
Guest Editor

Manuscript Submission Information

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  • mitochondrial dynamics
  • mitophagy
  • mitochondrial fusion
  • mitochondrial fission
  • oxidative stress
  • acute kidney injury
  • chronic kidney disease
  • inflammation
  • kidney fibrosis

Published Papers (1 paper)


24 pages, 1681 KiB  
Systematic Review
Mitochondrial Dysfunction in Individuals with Diabetic Kidney Disease: A Systematic Review
Cells 2022, 11(16), 2481; - 10 Aug 2022
Cited by 2 | Viewed by 2321
Mitochondrial dysfunction is implicated in the pathogenesis of diabetic kidney disease (DKD). Compared to the vast body of evidence from preclinical in vitro and in vivo studies, evidence from human studies is limited. In a comprehensive search of the published literature, findings from [...] Read more.
Mitochondrial dysfunction is implicated in the pathogenesis of diabetic kidney disease (DKD). Compared to the vast body of evidence from preclinical in vitro and in vivo studies, evidence from human studies is limited. In a comprehensive search of the published literature, findings from studies that reported evidence of mitochondrial dysfunction in individuals with DKD were examined. Three electronic databases (PubMed, Embase, and Scopus) were searched in March 2022. A total of 1339 articles were identified, and 22 articles met the inclusion criteria. Compared to non-diabetic controls (NDC) and/or individuals with diabetes but without kidney disease (DC), individuals with DKD (age ~55 years; diabetes duration ~15 years) had evidence of mitochondrial dysfunction. Individuals with DKD had evidence of disrupted mitochondrial dynamics (11 of 11 articles), uncoupling (2 of 2 articles), oxidative damage (8 of 8 articles), decreased mitochondrial respiratory capacity (1 of 1 article), decreased mtDNA content (5 of 6 articles), and decreased antioxidant capacity (3 of 4 articles) compared to ND and/or DC. Neither diabetes nor glycemic control explained these findings, but rather presence and severity of DKD may better reflect degree of mitochondrial dysfunction in this population. Future clinical studies should include individuals closer to diagnosis of diabetes to ascertain whether mitochondrial dysfunction is implicated in the development of, or is a consequence of, DKD. Full article
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