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month download article/chapter doxorubicin-induced acute cardiotoxicity dox-treated mouse hearts chemotherapy drug-induced nephrotoxicity doxorubicin-induced cardiomyocyte panoptosis pi3k/akt mediated suppression inflammation-related signaling pathways akt/nrf2-dependent manner akt/nrf2 signaling cascade dox-induced cardiotoxicity doxorubicin-induced cardiotoxicity doxorubicin-induced cardiomyopathy cellular biochemistry aims acute lung injury rip3 dependent necroptosis jun ren revised full article pdf prevent doxorubicin cardiomyopathy related subjects privacy choices/manage cookies doxorubicin-induced toxicity ma zg facilitates myocardial hypertrophy promote myocardial survival promoting oxidative stress moderating oxidative stress elevated oxidative stress reducing oxidative stress inhibiting oxidative stress ischemic dilated cardiomyopathy mediated nrf2 activation receptor pyrin domain zhenyi wang wrote outstanding youth foundation nlrp3 inflammasome activation jiao tong university laboratory animal center holds exclusive rights nrf2-mediated pathway european economic area reducing racial disparities nat rev cardiol lps-stimulated microglia ischemic stroke rats muscle lim protein additional information publisher' conditions privacy policy chinese materia medica pre-clinical therapeuticapproaches danger signal sensor

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         headline:RIP3 orchestrates oxidative stress and pyroptosis in doxorubicin-induced cardiotoxicity through regulation of AKT/Nrf2 signaling cascade
         description:This study was designed to explore the role of RIP3 in DOX-induced cardiotoxicity and its underlying molecular mechanisms. Our results demonstrate that RIP3 exacerbates DOX-induced cardiotoxicity through promoting oxidative stress and pyroptosis by regulating the AKT/Nuclear factor erythroid 2-related factor 2 (Nrf2) signal pathway. Inhibition of RIP3 using GSK-872 attenuated DOX-induced cardiac remodeling and contractile dysfunction. Moreover, using GSK-872 in vivo, the results revealed that inhibition of RIP3 alleviated DOX-induced cardiotoxicity by the resulting inhibition of oxidative stress and pyroptosis. In addition, inhibition of RIP3 increased the protein levels of AKT and Nrf2 in DOX-treated mouse hearts. Furthermore, the AKT inhibitor LY294002 lessened RIP3 reduction-offered protection against DOX-induced H9c2 cell injury by moderating oxidative stress and pyroptosis. Taken together, these data demonstrate that RIP3 activation orchestrates DOX-induced cardiotoxicity through elevated oxidative stress and pyroptosis in an AKT/Nrf2-dependent manner. Those findings highlight the clinical relevance and therapeutic potential of targeting RIP3 for the treatment of DOX-induced cardiotoxicity.
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      headline:RIP3 orchestrates oxidative stress and pyroptosis in doxorubicin-induced cardiotoxicity through regulation of AKT/Nrf2 signaling cascade
      description:This study was designed to explore the role of RIP3 in DOX-induced cardiotoxicity and its underlying molecular mechanisms. Our results demonstrate that RIP3 exacerbates DOX-induced cardiotoxicity through promoting oxidative stress and pyroptosis by regulating the AKT/Nuclear factor erythroid 2-related factor 2 (Nrf2) signal pathway. Inhibition of RIP3 using GSK-872 attenuated DOX-induced cardiac remodeling and contractile dysfunction. Moreover, using GSK-872 in vivo, the results revealed that inhibition of RIP3 alleviated DOX-induced cardiotoxicity by the resulting inhibition of oxidative stress and pyroptosis. In addition, inhibition of RIP3 increased the protein levels of AKT and Nrf2 in DOX-treated mouse hearts. Furthermore, the AKT inhibitor LY294002 lessened RIP3 reduction-offered protection against DOX-induced H9c2 cell injury by moderating oxidative stress and pyroptosis. Taken together, these data demonstrate that RIP3 activation orchestrates DOX-induced cardiotoxicity through elevated oxidative stress and pyroptosis in an AKT/Nrf2-dependent manner. Those findings highlight the clinical relevance and therapeutic potential of targeting RIP3 for the treatment of DOX-induced cardiotoxicity.
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