Mitochondrial energetics in the kidney
By P. Bhargava, R. Schnellmann. Nature Reviews Nephrology, 2017
1,186 citations recorded by the source corpus.
The kidney requires a large number of mitochondria to remove waste from the blood and regulate fluid and electrolyte balance. Mitochondria provide the energy to drive these important functions and can adapt to different metabolic conditions through a number of signalling pathways (for example, mechanistic target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK) pathways) that activate the transcriptional co-activator peroxisome proliferator-activated receptor-γ co-activator 1α (PGC1α), and by balancing mitochondrial dynamics and energetics to maintain mitochondrial homeostasis. Mitochondrial dysfunction leads to a decrease in ATP production, alterations in cellular functions and structure, and the loss of renal function. Persistent mitochondrial dysfunction has a role in the early stages and progression of renal diseases, such as acute kidney injury (AKI) and diabetic nephropathy, as it disrupts mitochondrial homeostasis and thus normal kidney function. Improving mitochondrial homeostasis and function has the potential to restore renal function, and administering compounds that stimulate mitochondrial biogenesis can restore mitochondrial and renal function in mouse models of AKI and diabetes mellitus. Furthermore, inhibiting the fission protein dynamin 1-like protein (DRP1) might ameliorate ischaemic renal injury by blocking mitochondrial fission.
Subfields: Clinical Biochemistry, Molecular Biology, Nephrology
View Paper: https://www.semanticscholar.org/paper/769f49c7f46f9f0d3bedce98ed58c15283a36d10
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Citations in the corpus
- Mitochondrial ROS promote mitochondrial dysfunction and inflammation in ischemic acute kidney injury by disrupting TFAM-mediated mtDNA maintenance (2021, background): “Although excessive mtROS have been shown to disturb multiple pathways involved in calcium homeostasis, mitochondrial permeability, and cytochrome C release and to directly induce renal cell death [3,38,39], their specific roles in mitochondrial damage and inflammation during IRI-AKI are not complete”