ArticleAmerican journal of physiology. Renal physiology2008
Akt activation improves oxidative phosphorylation in renal proximal tubular cells following nephrotoxicant injury.
Article in American journal of physiology. Renal physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
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- Cellular and mitochondrial taurine depletion in bile duct ligated rats: a justification for taurine supplementation in cholestasis/cirrhosis.Clinical and experimental hepatology · 2022Article
- The sugar daddy: the role of the renal proximal tubule in glucose homeostasis.American journal of physiology. Cell physiology · 2022Review
- Impacts of Oxidative Stress and PI3K/AKT/mTOR on Metabolism and the Future Direction of Investigating Fucoidan-Modulated Metabolism.Antioxidants (Basel, Switzerland) · 2022Review
- Cysteine as a Multifaceted Player in Kidney, theMolecules (Basel, Switzerland) · 2022Review
- Tourniquet-induced lower limb ischemia/reperfusion reduces mitochondrial function by decreasing mitochondrial biogenesis in acute kidney injury in mice.Physiological reports · 2022Article
- γ-Tocotrienol Protects against Mitochondrial Dysfunction, Energy Deficits, Morphological Damage, and Decreases in Renal Functions after Renal Ischemia.International journal of molecular sciences · 2021Article
- Synchronous effects of targeted mitochondrial complex I inhibitors on tumor and immune cells abrogate melanoma progression.iScience · 2021Article
- Deletion of VDAC1 Hinders Recovery of Mitochondrial and Renal Functions After Acute Kidney Injury.Biomolecules · 2020Article
- The potential role of mitochondrial impairment in the pathogenesis of imatinib-induced renal injury.Heliyon · 2019Article
- AKT-mediated phosphorylation of ATG4B impairs mitochondrial activity and enhances the Warburg effect in hepatocellular carcinoma cells.Autophagy · 2018Article
- Deletion of protein kinase C-ε attenuates mitochondrial dysfunction and ameliorates ischemic renal injury.American journal of physiology. Renal physiology · 2017Article
- Glycoprotein Ib activation by thrombin stimulates the energy metabolism in human platelets.PloS one · 2017Article
- The proliferation impairment induced by AQP3 deficiency is the result of glycerol uptake and metabolism inhibition in gastric cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Random Effects Model for Multiple Pathway Analysis with Applications to Type II Diabetes Microarray Data.Statistics in biosciences · 2015Article
- Computer-aided targeting of the PI3K/Akt/mTOR pathway: toxicity reduction and therapeutic opportunities.International journal of molecular sciences · 2014Review
- Protein kinase C-α interaction with iHSP70 in mitochondria promotes recovery of mitochondrial function after injury in renal proximal tubular cells.American journal of physiology. Renal physiology · 2013Article
- Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) signaling regulates mitochondrial biogenesis and respiration via estrogen-related receptor α (ERRα).The Journal of biological chemistry · 2013Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
Previously, we showed that protein kinase B (Akt) activation increases intracellular ATP levels and decreases necrosis in renal proximal tubular cells (RPTC) injured by the nephrotoxicant S-(1, 2-dichlorovinyl)-l-cysteine (DCVC) (Shaik ZP, Fifer EK, Nowak G. Am J Physiol Renal Physiol 292: F292-F303, 2007). This study examined the role of Akt in improving mitochondrial function in DCVC-injured RPTC. Our data show a novel observation that phosphorylated (active) Akt is localized in mitochondria of noninjured RPTC, both in mitoplasts and the mitochondrial outer membrane. Mitochondrial levels of active Akt decreased in nephrotoxicant-injured RPTC, and this decrease was associated with mitochondrial dysfunction. DCVC decreased basal, uncoupled, and state 3 respirations; ATP production; activities of complexes I, II, and III; the mitochondrial membrane potential (DeltaPsi(m)); and F(0)F(1)-ATPase activity. Expressing constitutively active Akt in DCVC-injured RPTC increased the levels of phosphorylated Akt in mitochondria, reduced the decreases in basal and uncoupled respirations, increased complex I-coupled state 3 respiration and ATP production, enhanced activities of complex I, complex III, and F(0)F(1)-ATPase, and improved DeltaPsi(m). In contrast, inhibiting Akt activation by expressing dominant negative (inactive) Akt or using 20 microM LY294002 exacerbated decreases in electron transport rate, state 3 respiration, ATP production, DeltaPsi(m), and activities of complex I, complex III, and F(0)F(1)-ATPase. In conclusion, our data show that Akt activation promotes mitochondrial respiration and ATP production in toxicant-injured RPTC by 1) improving integrity of the respiratory chain and maintaining activities of complex I and complex III, 2) reducing decreases in DeltaPsi(m), and 3) restoring F(0)F(1)-ATPase activity.
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