about
Reactive oxygen species, nutrition, hypoxia and diseases: Problems solved?Evidence for a common mechanism of SIRT1 regulation by allosteric activatorsDeclining NAD(+) induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during agingInhibitory effect of carvedilol in the high-conductance state of the mitochondrial permeability transition pore.Role of mitochondrial dysfunction in combined bile acid-induced cytotoxicity: the switch between apoptosis and necrosis.European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS).High-fat and obesogenic diets: current and future strategies to fight obesity and diabetes.SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial functionThe Role of microRNAs in Mitochondria: Small Players Acting Wide.Losartan activates sirtuin 1 in rat reduced-size orthotopic liver transplantation.Mitochondrially-mediated toxicity of bile acids.Berberine protects against high fat diet-induced dysfunction in muscle mitochondria by inducing SIRT1-dependent mitochondrial biogenesis.Diabetes and mitochondrial function: role of hyperglycemia and oxidative stress.GSK3β and VDAC Involvement in ER Stress and Apoptosis Modulation during Orthotopic Liver Transplantation.Regulation of mitochondrial biogenesis in metabolic syndrome.Hepatic FXR: key regulator of whole-body energy metabolism.Role of oxidative stress in the pathogenesis of nonalcoholic steatohepatitis.The NAD ratio redox paradox: why does too much reductive power cause oxidative stress?Regulation of Mitochondrial Function and its Impact in Metabolic Stress.An autophagic process is activated in HepG2 cells to mediate BDE-100-induced toxicity.The bile acid chenodeoxycholic acid directly modulates metabolic pathways in white adipose tissue in vitro: insight into how bile acids decrease obesity.Mitochondrial bioenergetics and posthepatectomy liver dysfunction.The P2X7 receptor antagonist Brilliant Blue G attenuates contralateral rotations in a rat model of Parkinsonism through a combined control of synaptotoxicity, neurotoxicity and gliosis.Therapeutic concentrations of mitoxantrone elicit energetic imbalance in H9c2 cells as an earlier event.Exposure to dibenzofuran triggers autophagy in lung cells.Low-dose, subchronic exposure to silver nanoparticles causes mitochondrial alterations in Sprague-Dawley rats.Hyperglycemia decreases mitochondrial function: the regulatory role of mitochondrial biogenesis.Lack of Additive Effects of Resveratrol and Energy Restriction in the Treatment of Hepatic Steatosis in RatsAdenosine receptors: regulatory players in the preservation of mitochondrial function induced by ischemic preconditioning of rat liver.PPARα Agonist WY-14643 Induces SIRT1 Activity in Rat Fatty Liver Ischemia-Reperfusion Injury.Hepatic and skeletal muscle mitochondrial toxicity of chitosan oligosaccharides of normal and diabetic rats.Reduction in cardiac mitochondrial calcium loading capacity is observable during alpha-naphthylisothiocyanate-induced acute cholestasis: a clue for hepatic-derived cardiomyopathies?Indirubin-3'-oxime prevents hepatic I/R damage by inhibiting GSK-3beta and mitochondrial permeability transition.Sirtuin 1 in rat orthotopic liver transplantation: an IGL-1 preservation solution approach.Exposure to 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin and tetraethyl lead affects lung mitochondria bioenergetics.Protective effect of carvedilol on chenodeoxycholate induction of the permeability transition pore.Interactions of combined bile acids on hepatocyte viability: cytoprotection or synergism.Improved efficiency of hepatic mitochondrial function in rats with cholestasis induced by an acute dose of alpha-naphthylisothiocyanate.Enhanced permeability transition explains the reduced calcium uptake in cardiac mitochondria from streptozotocin-induced diabetic rats.Mitochondrially mediated synergistic cell killing by bile acids.
P50
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P50
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Anabela Pinto Rolo
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Anabela Pinto Rolo
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P106
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7003333455
P21
P31
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0000-0003-3535-9630