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Topics {✒️}

high-fat-diet-induced insulin resistance hydrocinnamoyl-l-valylpyrrolidine sglt-2i impairing nrf2/brg1/ho-1 signaling inositol-requiring enzyme 1α springer nature impairing caveolin-3-modulated pi3k/akt brain-derived neurotrophic factor high-lipid-induced inflammatory injury cav-3-mg53-pi3k complex-mediated activation attenuates lipopolysaccharide-induced injury cav-3/insulin receptor-β complex additional information publisher impairing adipor1/caveolin-3/stat3 signaling ampk/akt/enos signalling pathway disc-shaped oligomeric complex hypoxia/reoxygenation-induced apoptosis pi3k/akt-dependent signaling pathway disc-shaped oligomeric complexes δ-opioid-induced cardioprotection /tropomyosin-related kinase receptor tropomyosin-related kinase receptor hyperglycemia-induced protein kinase puerarin attenuates high-glucose limb-girdle muscular dystrophy bmc cardiovasc disor tir/bb-loop mimetic cardiac ischemia/reperfusion injury ischemia/reperfusion cardiac injury cardiac ischemia-reperfusion injury hyperglycemia-induced oxidative stress cardiac ischaemia/reperfusion injury remifentanil preconditioning-induced protection acute ischemia/reperfusion injury glycogen synthase kinase-3β myocardial ischemia-reperfusion injury myocardial ischemia/reperfusion injury α-linolenic acid b-cell population-percentage long-term diabetes impairs /r-induced er stress /r-induced myocardial injury brg1/nrf2/stat3 signalling myocardial iischemia/reperfusion injury ischemia-reperfused rat heart lipid-binding protein consisting stimulating pi3k/akt pathway isoflurane-induced cardiac protection t-cell cytokine production ampk-opa1 signaling pathways bcl-2-interacting protein1

Questions {❓}

• Cardioprotection by selective SGLT-2 inhibitors in a non-diabetic mouse model of myocardial ischemia/reperfusion injury: a class or a drug effect?

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         headline:Caveolin-3: therapeutic target for diabetic myocardial ischemia/reperfusion injury
         description:Myocardial ischemia/reperfusion (I/R) injury is a major global health problem with high rates of mortality and disability, which is more severe in patients with diabetes. Substantial researches have documented that diabetic myocardium are more susceptible to I/R injury, but many current intervention strategies against myocardial I/R injury have limited effectiveness in diabetic hearts. Caveolin-3 (Cav-3) is the signature protein of caveolae and serves as a signal integration and transduction platform in the plasma membrane of cardiomyocytes, which plays a vital role in myocardial functions, metabolism and protection of multiple conditioning strategies against I/R injury. Nevertheless, numerous studies have revealed that the expression of Cav-3 is impaired in diabetic hearts, which contributes to increased vulnerability of myocardium to I/R injury and resistance to protective conditioning strategies. In this review, we outline the basic structure and function of Cav-3, emphatically present the unique role of Cav-3 as a signal integration and transduction element in diabetic myocardial I/R injury and discuss its therapeutic perspective in strategies against myocardial I/R injury in diabetes.
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      headline:Caveolin-3: therapeutic target for diabetic myocardial ischemia/reperfusion injury
      description:Myocardial ischemia/reperfusion (I/R) injury is a major global health problem with high rates of mortality and disability, which is more severe in patients with diabetes. Substantial researches have documented that diabetic myocardium are more susceptible to I/R injury, but many current intervention strategies against myocardial I/R injury have limited effectiveness in diabetic hearts. Caveolin-3 (Cav-3) is the signature protein of caveolae and serves as a signal integration and transduction platform in the plasma membrane of cardiomyocytes, which plays a vital role in myocardial functions, metabolism and protection of multiple conditioning strategies against I/R injury. Nevertheless, numerous studies have revealed that the expression of Cav-3 is impaired in diabetic hearts, which contributes to increased vulnerability of myocardium to I/R injury and resistance to protective conditioning strategies. In this review, we outline the basic structure and function of Cav-3, emphatically present the unique role of Cav-3 as a signal integration and transduction element in diabetic myocardial I/R injury and discuss its therapeutic perspective in strategies against myocardial I/R injury in diabetes.
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Analytics and Tracking {📊}

• Google Tag Manager

Libraries {📚}

• Prism.js

CDN Services {📦}

• Crossref