Chemotherapy-induced cardiotoxicity and mitigation

This study shows that dietary nitrate and nitrite reduce cardiac fibrosis and oxidative damage in tumor-bearing mice treated with doxorubicin without affecting tumor response.

This study shows that AICAr protects cardiomyocytes from doxorubicin toxicity by inhibiting autophagy, increasing p62, and enhancing NRF2 activity through ADK-dependent mechanisms.

This study shows CARP protects against doxorubicin-induced cardiotoxicity by maintaining mitochondrial homeostasis through NRF1 signaling.

This study shows anthracyclines alter chromatin accessibility in cardiomyocytes, overlapping with cardiovascular disease risk loci.

This study evaluates HM12, a calcium channel inhibitor, for cardioprotective effects against doxorubicin toxicity in rats, showing improved antioxidant status and reduced inflammation.

This study shows ATF4 protects against doxorubicin-induced cardiomyopathy by enhancing H2S-mediated antioxidation through upregulation of CSE.

The paper introduces KICDB, a database that integrates transcriptomic and causal inference data to explore the mechanisms of kinase inhibitor-induced cardiotoxicity.

This study develops an advanced cardiac organoid model with fibroblast-driven ECM self-secretion to better mimic adult cardiac physiology and assess doxorubicin-induced cardiotoxicity.

This study shows that Rac1 deletion reduces anthracycline-induced organ damage in mice, with effects varying by organ and drug type.

This study compares the response of murine embryonic stem cells and their endothelial progeny to doxorubicin and DNA repair inhibitors, finding differential susceptibility and functional impairments in differentiated cells.

This study shows that low-dose doxorubicin treatment of human iPSCs causes mitochondrial dysfunction and transcriptional changes that impair cardiac regeneration in derived cardiomyocytes.

This study identifies serum and plasma sphingolipids as potential biomarkers for anthracycline-induced cardiotoxicity, showing correlations with cardiac outcomes during and after therapy.

This study identifies transcriptomic changes in a rat model of doxorubicin-induced cardiotoxicity, revealing metabolic dysregulation and circadian rhythm disruption that may inform early diagnostic biomarkers.

This study identifies nSMase2 as a critical mediator of Doxorubicin-induced cardiotoxicity and shows its loss protects against cardiac damage.

This study shows malonate prevents chemotherapy-induced cardiotoxicity by inhibiting mitochondrial reverse electron transport, preserves cardiac function, and sensitizes AML cells to intensive chemotherapy.

This study evaluates anthracycline-induced arterial injury in non-human primates and lymphoma patients using histopathology and PET/CT, finding increased fibrosis in primates but no inflammation in patients.

The paper identifies cardiotoxic drug signatures using bulk transcriptomics and integrates them with genomic and single-cell data to predict toxicity mechanisms.

This study shows that inhibiting Cyp1a protects mice from anthracycline-induced cardiomyopathy by reducing cardiac dysfunction and altering gene expression related to mitophagy and inflammation.

The paper investigates the shared gene expression response to TOP2-inhibiting breast cancer drugs in cardiomyocytes and identifies genetic factors associated with inter-individual variation in cardiotoxicity.

The paper introduces IVCCA, a bioinformatics tool to identify drug targets for oxaliplatin-induced cardiotoxicity without affecting cancer treatment, finding new pathways like energy metabolism as potential therapeutic targets.

The paper identifies genetic markers for anthracycline-induced cardiotoxicity risk by analyzing intermediate molecular phenotypes in mice and human cohorts.

This study shows that remote ischemic preconditioning (RIPC) before doxorubicin injections reduces cardiotoxicity by preserving mitochondrial integrity and cardiac function in pigs.

This study identifies SIRT6 as a non-enzymatic coactivator of GATA4 that protects against doxorubicin-induced cardiotoxicity by enhancing GATA4 acetylation through recruitment of Tip60.

This study identifies RXRA as a therapeutic target for doxorubicin-induced cardiomyopathy in zebrafish by showing its endothelial-specific function and response to FDA-approved agonists.

This study identifies genetic variants influencing the transcriptomic response to doxorubicin in cardiomyocytes and links them to anthracycline-induced cardiotoxicity risk.