Mitochondrial energetics in the kidney
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TLDR
Implementing compounds that stimulate mitochondrial biogenesis can restore mitochondrial and renal function in mouse models of AKI and diabetes mellitus and inhibiting the fission protein dynamin 1-like protein (DRP1) might ameliorate ischaemic renal injury by blocking mitochondrial fission.Abstract:
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.read more
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Metabolic Alterations in SARS-CoV-2 Infection and Its Implication in Kidney Dysfunction
Magaiver Andrade Silva,Magaiver Andrade Silva,Ana Ruth Paolinetti Alves da Silva,Mariana Abrantes do Amaral,Matheus Garcia Fragas,Niels Olsen Saraiva Câmara,Niels Olsen Saraiva Câmara +6 more
TL;DR: In this article, the authors explored the metabolism and its interface with SARS-CoV-2 infection and raised the perspective on metabolism disturbances as a critical event to kidney dysfunction in COVID-19.
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Gokhan Burcin Kubat,Mehmet Ozler,Oner Ulger,Özgür Ekinci,Ozbeyen Atalay,Ertugrul Celik,Mukerrem Safali,Murat Timur Budak +7 more
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Ludmila F M F Cardozo,Livia Alvarenga,Marcia Ribeiro,Lu Dai,Paul G. Shiels,Peter Stenvinkel,Bengt Lindholm,Denise Mafra +7 more
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Genome-Wide Association Studies of Metabolite Concentrations (mGWAS): Relevance for Nephrology.
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Labile Heme Aggravates Renal Inflammation and Complement Activation After Ischemia Reperfusion Injury.
Li Wang,Vijith Vijayan,Mi-Sun Jang,Anja Thorenz,Robert Greite,Song Rong,Rongjun Chen,Nelli Shushakova,Igor Tudorache,Katja Derlin,Pooja Pradhan,Kukuh Madyaningrana,Nodir Madrahimov,Jan Hinrich Bräsen,Ralf Lichtinghagen,Cees van Kooten,Markus Huber-Lang,Hermann Haller,Stephan Immenschuh,Faikah Gueler +19 more
TL;DR: Data show that prolonged duration of warm ischemia time increased labile heme levels in the kidney, which correlates with IRI-dependent inflammation and up-regulation of anaphylatoxin receptor expression.
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