SIRT3 a Major Player in Attenuation of Hepatic Ischemia‐Reperfusion Injury by Reducing ROS via Its Downstream Mediators: SOD2, CYP‐D, and HIF‐1<i>α</i>

Katwal, Gaurav; Baral, Dilip; Fan, Xiaoli; He, Weiyang; Zhang, Xinjiang; Li, Ling; Xiong, Yan; Ye, Qifa; Wang, Yanfeng

doi:10.1155/2018/2976957

Cited by 61 publications

(45 citation statements)

References 124 publications

(171 reference statements)

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“…SIRT3 exerts protective effects on mitochondria against oxidative stress. SIRT3 deacetylates the critical antioxidant enzyme manganese superoxide dismutase 2 (SOD2) at two different lysine sites to enhance its ROS-scavenging capability in mitochondrial matrix [ [123] , [124] , [125] ]. SIRT6 modifies the histones via deacetylation in the promoter regions of NF-κB–activated genes to further inhibit the proinflammatory response [ 126 ].…”

Section: Oxidative Stress and Epigenetic Modifications In Diabetic Rementioning

confidence: 99%

Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications

2020

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Oxidative stress, a cytopathic outcome of excessive generation of ROS and the repression of antioxidant defense system for ROS elimination, is involved in the pathogenesis of multiple diseases, including diabetes and its complications. Retinopathy, a microvascular complication of diabetes, is the primary cause of acquired blindness in diabetic patients. Oxidative stress has been verified as one critical contributor to the pathogenesis of diabetic retinopathy. Oxidative stress can both contribute to and result from the metabolic abnormalities induced by hyperglycemia, mainly including the increased flux of the polyol pathway and hexosamine pathway, the hyper-activation of protein kinase C (PKC) isoforms, and the accumulation of advanced glycation end products (AGEs). Moreover, the repression of the antioxidant defense system by hyperglycemia-mediated epigenetic modification also leads to the imbalance between the scavenging and production of ROS. Excessive accumulation of ROS induces mitochondrial damage, cellular apoptosis, inflammation, lipid peroxidation, and structural and functional alterations in retina. Therefore, it is important to understand and elucidate the oxidative stress-related mechanisms underlying the progress of diabetic retinopathy. In addition, the abnormalities correlated with oxidative stress provide multiple potential therapeutic targets to develop safe and effective treatments for diabetic retinopathy. Here, we also summarized the main antioxidant therapeutic strategies to control this disease.

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Section: Oxidative Stress and Epigenetic Modifications In Diabetic Rementioning

confidence: 99%

Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications

2020

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“…18 Reactive oxygen species (ROS) are increased during HIRI and studies have demonstrated that ROS may induce various forms of insulin resistance. 19 The use of antioxidants is believed to represent an effective treatment for insulin resistance. 20,21 As a commonly used intravenous anesthetic, propofol has a strong antioxidant capacity, and may improve the antioxidant capacity of red blood cells and tissues in rats.…”

Section: Discussionmentioning

confidence: 99%

Effect of propofol on the skeletal muscle insulin receptor in rats with hepatic ischemia-reperfusion injury

et al. 2019

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Objective: To investigate the effect of propofol on the expression and phosphorylation of the skeletal muscle insulin receptor and its substrates following hepatic ischemia-reperfusion injury (HIRI). Methods: Sixty healthy Wistar rats were divided randomly into a propofol group (P) and an ischemia-reperfusion group (I/R). Rats in the P group received propofol infusion prior to ischemia and during a 120-minute post-reperfusion period. Plasma glucose and insulin concentrations were measured, as well as expression levels of the insulin signaling proteins insulin receptor (IR) b unit (IRb) and IR substrate 1 (IRS-1). In addition, tyrosine phosphorylation levels of these proteins were measured in skeletal muscle. Results: Plasma glucose levels in the two groups were higher at 2 hours after reperfusion (T2) versus exposure of the hepatic hilum (T1). Plasma glucose levels in the I/R group were higher than those in the P group, while insulin levels at T2 were lower. In addition, phosphotyrosine levels of IRb and IRS-1 were decreased by 32.1% and 22.4%, respectively. Conclusion: Propofol increased phosphotyrosine levels of IRb and IRS-2, resulting in an alleviation of increased plasma glucose levels following HIRI.

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“…Studies have found the PI3K/Akt pathway is associated with cardiomyocytes apoptosis induced by I/R [36,37]. Some investigation found that HIF-1α participated in I/R injury in multiple organs as a critical modulator [38,39]. Liu and his colleagues found that DMY decreased the apoptosis and necrosis by I/R treatment, and PI3K/Akt and HIF-1α plays a crucial role in protection during this process.…”

Section: Bioinformatic Analysis and Luciferase Assay In The Present Smentioning

confidence: 99%

Overexpression of Long noncoding RNA Oprm1 Attenuates Myocardial Ischemia/Reperfusion Injury by Increasing Endogenous Hydrogen Sulfide Production via Oprm1/miR-30b-5p/CSE axis

Hu¹,

Liu²,

Wu³

et al. 2020

Preprint

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Background: Ischemia/Reperfusion (I/R) Injury largely limits the efficacy of revascularization in acute myocardial infarction. Long noncoding RNA (lncRNA) Oprm1 is protective in cerebral I/R injury. However, the effect of lncRNA Oprm1 on myocardial I/R injury and its mechanism remains unknown.Methods: We ligated and then released the left anterior descending coronary artery of adult male rats to build the I/R model in vivo, while an H9c2 cardiomyocytes hypoxia-reoxygenation (H/R) model was also used. Myocardial infarction area, cardiac function, histology, Tunnel staining, cell viability, and vital protein expression was conducted and compared.Results: lncRNA Oprm1 was significantly down-regulated in the I/R injury model. When administered with the AAV9-Oprm1 vector, the myocardial injury and cardiac function were mitigated and preserved, with apoptosis reduced. The cystathionine-γ-lyase (CSE) expression and hydrogen sulfide (H2S) expression were increased. The dual-luciferase reporter gene revealed the targeted relationship between lncRNA Oprm1 and miR-30b-5p. In H9c2 cardiomyocytes models, the miR-30b-5p blocked the protective effect of lncRNA Oprm1 on H/R injury, when Bcl-2, Bcl-xl was down-regulated, and HIF-1α, Bnip-3, Caspase-3, and Caspase-9 up-regulated.Conclusions: lncRNA Oprm1can competitively combines with miR-30b-5p, which down-regulates the expression of CSE. When administered with lncRNA Oprm1, increased endogenous H2S can reduce apoptosis and protect the myocardium from I/R injury via activating PI3K/Akt pathway and inhibiting HIF1-α activity.

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SIRT3 a Major Player in Attenuation of Hepatic Ischemia‐Reperfusion Injury by Reducing ROS via Its Downstream Mediators: SOD2, CYP‐D, and HIF‐1α

Cited by 61 publications

References 124 publications

Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications

Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications

Effect of propofol on the skeletal muscle insulin receptor in rats with hepatic ischemia-reperfusion injury

Overexpression of Long noncoding RNA Oprm1 Attenuates Myocardial Ischemia/Reperfusion Injury by Increasing Endogenous Hydrogen Sulfide Production via Oprm1/miR-30b-5p/CSE axis

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