{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nicol M"],"funding":["Fondation de France"],"pagination":["8104"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11890863"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["Late-onset cardiotoxicity induced by anthracyclines occurs years to decades after completion of anti-cancer therapy and is associated with increased morbi-mortality of cancer survivors. Chemotherapy at the time of treatment probably causes cardiac damages for which the juvenile heart compensate. Co-morbidities happening in the adulthood such as type 1 diabetes (DT1), affect the heart and thus can unmask chemotherapy induced cardiotoxicity. To prove our hypothesis, we induced hyperglycemia [Streptozotocin treatment (STZ), 50 mg/kg/day for 5 days] in 11 weeks old mice who previously received doxorubicin treatment (Dox, 3 mg/kg) when they were six-weeks old. Interestingly, streptozotocin-induced hyperglycemia in Dox-pretreated mice (Dox-STZ) induced a higher mortality (p < 0.05) and more severe cardiac dysfunction (p < 0.0001) when compared with mice receiving Dox or STZ alone. Apoptosis evaluated by caspase 3 protein expression and Bax/Bcl2 genes expression was higher in Dox-STZ mice compared to STZ or Dox alone. While Dox and STZ independently induced capillary rarefaction, cardiomyocytes atrophy was only induced by STZ. Furthermore, Sirius-red staining of cardiac sections showed higher fibrosis levels (p < 0.0001) in Dox-STZ compared to Dox or STZ alone. All together, these results demonstrate that STZ precipitates and unmask cardiac dysfunction in previously treated Dox animals."],"journal":["Scientific reports"],"pubmed_title":["Streptozotocin-induced hyperglycemia unmasks cardiotoxicity induced by doxorubicin."],"pmcid":["PMC11890863"],"funding_grant_id":["2019 00086501"],"pubmed_authors":["Genest M","Azibani F","Polidano E","Samuel JL","Assad N","Nicol M","Rahli R","Deniau B","Mebazaa A","Solal AC"],"additional_accession":[]},"is_claimable":false,"name":"Streptozotocin-induced hyperglycemia unmasks cardiotoxicity induced by doxorubicin.","description":"Late-onset cardiotoxicity induced by anthracyclines occurs years to decades after completion of anti-cancer therapy and is associated with increased morbi-mortality of cancer survivors. Chemotherapy at the time of treatment probably causes cardiac damages for which the juvenile heart compensate. Co-morbidities happening in the adulthood such as type 1 diabetes (DT1), affect the heart and thus can unmask chemotherapy induced cardiotoxicity. To prove our hypothesis, we induced hyperglycemia [Streptozotocin treatment (STZ), 50 mg/kg/day for 5 days] in 11 weeks old mice who previously received doxorubicin treatment (Dox, 3 mg/kg) when they were six-weeks old. Interestingly, streptozotocin-induced hyperglycemia in Dox-pretreated mice (Dox-STZ) induced a higher mortality (p < 0.05) and more severe cardiac dysfunction (p < 0.0001) when compared with mice receiving Dox or STZ alone. Apoptosis evaluated by caspase 3 protein expression and Bax/Bcl2 genes expression was higher in Dox-STZ mice compared to STZ or Dox alone. While Dox and STZ independently induced capillary rarefaction, cardiomyocytes atrophy was only induced by STZ. Furthermore, Sirius-red staining of cardiac sections showed higher fibrosis levels (p < 0.0001) in Dox-STZ compared to Dox or STZ alone. All together, these results demonstrate that STZ precipitates and unmask cardiac dysfunction in previously treated Dox animals.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2025-04-04T08:23:24.8Z","creation":"2025-04-04T08:23:24.8Z"},"accession":"S-EPMC11890863","cross_references":{"pubmed":["40057546"],"doi":["10.1038/s41598-025-91824-0"]}}