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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Journal ArticleDOI
Empagliflozin improves diabetic renal tubular injury by alleviating mitochondrial fission via AMPK/SP1/PGAM5 pathway
Xiangyang Liu,Chaofei Xu,Linxin Xu,Xiaoyu Li,Hongxi Sun,Mei Xue,Ting Li,Xiaochen Yu,Bei Sun,Liming Chen +9 more
TL;DR: The PGAM5 aggravated the development of diabetic renal tubular injury and the Empa could improve the DKD by alleviating mitochondrial fission via AMPK/SP1/PGAM5 pathway.
Journal ArticleDOI
Targeting a Braf/Mapk pathway rescues podocyte lipid peroxidation in CoQ-deficiency kidney disease.
Eriene-Heidi Sidhom,Choah Kim,Choah Kim,Maria Kost-Alimova,May Theng Ting,Keith Keller,Julian Avila-Pacheco,Andrew J.B. Watts,Andrew J.B. Watts,Katherine A. Vernon,Katherine A. Vernon,Jamie L. Marshall,Estefanía Reyes-Bricio,Matthew Racette,Nicolas Wieder,Nicolas Wieder,Giulio Kleiner,Elizabeth J. Grinkevich,Fei Chen,Astrid Weins,Clary B. Clish,Jillian L. Shaw,Catarina M. Quinzii,Anna Greka,Anna Greka +24 more
TL;DR: It is demonstrated that CoQ depletion caused by Pdss2 enzyme deficiency in podocytes results in perturbations in polyunsaturated fatty acid (PUFA) metabolism and the Braf/Mapk pathway, rather than ETC dysfunction.
Journal ArticleDOI
Acute Kidney Disease to Chronic Kidney Disease.
TL;DR: In this article, the authors defined acute kidney disease (AKD) as the post-AKI status of acute or sub-acute kidney damage/dysfunction manifested by persistence of AKI beyond 7 to 90 days after the initial AKI diagnosis.
Journal ArticleDOI
Mechanisms of Synergistic Interactions of Diabetes and Hypertension in Chronic Kidney Disease: Role of Mitochondrial Dysfunction and ER Stress
TL;DR: The synergistic effects of HT and DM to promote kidney injury may be mediated by increased intraglomerular pressure and chronic activation of mechanotransduction signaling may amplify metabolic effects of DM causing cellular injury through a vicious cycle of impaired Ca2+ homeostasis, mitochondrial dysfunction, and ER stress.
Journal ArticleDOI
Mitoquinone Protects Podocytes from Angiotensin II-Induced Mitochondrial Dysfunction and Injury via the Keap1-Nrf2 Signaling Pathway
TL;DR: In this paper, the effects of mitoquinone (MitoQ) on podocyte injury were examined both in vivo and in vitro, and the results demonstrated that MitoQ exerts a protective effect in Ang II-induced mitochondrial injury in podocytes via the Keap1-Nrf2 signaling pathway.
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