Mitochondrial Dysfunction in Kidney Diseases
A topical collection in Cells (ISSN 2073-4409). This collection belongs to the section "Autophagy".
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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 Topical Collection, 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
Collection Editor
Manuscript Submission Information
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Keywords
- mitochondrial dynamics
- mitophagy
- mitochondrial fusion
- mitochondrial fission
- oxidative stress
- acute kidney injury
- chronic kidney disease
- inflammation
- kidney fibrosis