Chemotherapy-induced cardiotoxicity and mitigation

Genetic Determinants of Cell-Type-Specific Responses to Cardiotoxic Chemotherapeutic Agents

The paper identifies genetic variants associated with cardiotoxic responses to chemotherapeutic drugs using single-cell RNA-seq and eQTL analysis.

Impaired active myocardial relaxation is the earliest sign of anthracycline cardiotoxicity and reflects selective injury of the cardiomyocyte surface

Doxorubicin-induced Cardiotoxicity is Propagated by Paracrine Signaling through Small Extracellular Vesicles

This study shows DOX-induced cardiotoxicity spreads via paracrine signaling through extracellular vesicles, with plasma EV miRNA profiles indicating risk stratification and potential biomarkers for early detection.

Cardiomyocyte-derived Wnt5a drives doxorubicin-induced cardiomyopathy by amplifying cellular senescence

This study identifies Wnt5a as a driver of doxorubicin-induced cardiomyopathy by amplifying cellular senescence through a Wnt5a-Fzd2 feed-forward axis.

HDAC inhibition via suberoylanilide hydroxamic acid (SAHA) ameliorates Doxorubicin-induced cardiotoxicity

This study shows that HDAC inhibition with SAHA reduces doxorubicin-induced cardiotoxicity by modulating Topo IIb and MEF2-dependent transcription.

Meta-analysis of genome-wide association studies of doxorubicin-induced arrhythmia identifies MMP16 and KCTD15 as risk loci

This study identifies genetic risk loci for doxorubicin-induced arrhythmia through GWAS meta-analysis and validates their functional relevance in human and zebrafish models.

AMPKγ2 Deacetylation Drives Nuclear Translocation and Doxorubicin-Induced Cardiomyopathy via Nucleolar Stress Signaling

This study identifies AMPKγ2 deacetylation as a driver of Doxorubicin-induced cardiomyopathy through nucleolar stress and p53-mediated apoptosis, suggesting HDAC inhibitors could mitigate cardiac toxicity.

The MEK inhibitor trametinib incurs mitochondrial injury and induces innate immune responses in the mouse heart

This study shows trametinib causes mitochondrial injury and innate immune activation in mouse hearts, leading to cardiomyopathy and heart failure.

Progressive suppression of DNA repair genes with persistent p53 activation in Doxorubicin-treated cardiomyocytes

The paper profiles gene expression in DOX-treated cardiomyocytes over time, identifying a chronic gene signature enriched for p53 target genes and DNA damage response genes.

Novel Cardiometabolic Factors Regulate Neurite Outgrowth in Cancer Chemotherapy-Induced Cardiotoxicity

This study identifies novel cardiometabolic factors that regulate neurite outgrowth and shows chemotherapy disrupts this cardiac-neuronal communication.

ReCardioids: a robust human heart organoid platform to model doxorubicin- and radiotherapy-induced cardiotoxicity

The paper develops reCardioids, a human heart organoid model, to study doxorubicin and radiotherapy-induced cardiotoxicity, showing improved cellular maturity and response to treatment.

Exercise prevents cardiac electrical remodeling in doxorubicin-treated female mice but does not provide cardioprotection in males.

This study shows exercise prevents DOX-induced electrical remodeling in female mice but not mechanical dysfunction, while males experience mechanical issues without exercise protection.

Disrupting the Feed-Forward Cycle of RyR1 Calcium Leak and Oxidative Stress Mitigates Doxorubicin-Induced Skeletal Myopathy

This study shows that doxorubicin causes skeletal muscle weakness by disrupting RyR1 calcium leak and oxidative stress, and that stabilizing the RyR1-FKBP12 complex with triazole compounds mitigates these effects.

Kinome profiling allows examination and prediction of kinase inhibitor cardiotoxicity

The paper uses proteomic kinome profiling and machine learning to predict kinase inhibitor cardiotoxicity by analyzing off-target kinase engagement and its association with cardiac adverse events.

Post-daunorubicin treatment effects on cardiovascular function in the Ts65Dn mouse model of Down syndrome

This study examines the chronic cardiovascular effects of daunorubicin in Ts65Dn mice, a model of Down syndrome, compared to wild-type mice, finding strain-specific differences in cardiac and vascular function.

β2-Adrenergic Signaling Switches from Cardioprotective to Cardiotoxic in Acute vs. Chronic Oxidative Stress

This study shows that β2-adrenergic receptor signaling is cardioprotective in acute oxidative stress but cardiotoxic in chronic stress, with implications for β-blocker use in cardiovascular disease.

Sex differences in cardiomyocyte proteomic responses to the cardiotoxic chemotherapy drug doxorubicin

The paper presents a proteomic dataset from rat cardiomyocytes treated with doxorubicin, identifying proteins regulated in young hearts and highlighting sex differences in cardiotoxicity.

Lipid A counteracts doxorubicin-induced systemic dysfunction by boosting mitochondrial activity

This study shows lipid A improves mitochondrial function and counteracts doxorubicin-induced heart failure and immune decline in mice.

Cardiac Reprogramming with Drug Resistance Alleviates Doxorubicin-induced Cardiotoxicity in Mice and Pigs

This paper introduces a strategy called TopCare to reduce doxorubicin-induced cardiotoxicity by temporarily increasing P-gp expression in cardiomyocytes, showing improved survival and cardiac function in mice and pigs.

PPP1R3G Deletion Blocks RIPK1-Mediated Apoptosis and Necroptosis in Doxorubicin-Induced Cardiotoxicity

This study identifies PPP1R3G as a critical amplifier of doxorubicin-induced cardiotoxicity by promoting RIPK1-mediated apoptosis and necroptosis.

DRP1 inhibition confers cardioprotection against doxorubicin while preserving anticancer efficacy

This paper shows DRP1 inhibition reduces doxorubicin-induced cardiotoxicity while maintaining its anticancer effects in multiple cancer models.

Conserved RNA-protein modules link early anthracycline responses to atrial fibrillation risk

The paper identifies RNA-protein modules linked to anthracycline-induced cardiotoxicity and atrial fibrillation risk through multi-omics integration.

A simplified co-culture reveals altered cardiotoxic responses to doxorubicin in hPSC-derived cardiomyocytes in the presence of endothelial cells

This study shows that endothelial cells enhance doxorubicin-induced cardiotoxicity in co-cultures with cardiomyocytes, challenging the focus on cardiomyocytes alone.

Integrated Omics Approach to Delineate the Mechanisms of Doxorubicin-Induced Cardiotoxicity

This study uses multi-omics analysis to identify molecular pathways and temporal changes in doxorubicin-induced cardiotoxicity in mice, revealing potential biomarkers for cardioprotection.

Endothelial RRM2B-dependent mitochondrial DNA signalling drives doxorubicin-cardiotoxicity

This study identifies endothelial RRM2B-dependent mitochondrial DNA signaling as a driver of doxorubicin-induced cardiotoxicity and shows that Eltrombopag can prevent it.

Topoisomerase II inhibitors CX-5461 and Doxorubicin differ in their cardiotoxicity profiles

This study compares the cardiotoxicity of CX-5461 and Doxorubicin in iPSC-derived cardiomyocytes, finding CX is less cytotoxic and induces fewer gene expression changes.

Empagliflozin alleviates doxorubicin-induced cardiotoxicity by suppressing oxidative stress via modulation of the JNK/Nrf2 signaling pathway

This study shows empagliflozin reduces doxorubicin-induced cardiotoxicity by modulating the JNK/Nrf2 pathway and decreasing oxidative stress in mice.

predicTox: An integrated database of clinical risk frequencies and human gene expression signatures for cardiotoxic drugs

The paper introduces predicTox, a database integrating clinical risk scores and gene expression data to identify genomic variants and pathways linked to drug-induced cardiotoxicity.

Phosphatidylserine-Based Liposomes Encapsulating DMX-5804 Protect Against Doxorubicin-Induced Cardiotoxicity

This study develops NanoDMX, a liposomal formulation of DMX-5804, which prevents doxorubicin-induced left ventricular dysfunction in mice and protects cardiomyocytes through non-JNK pathways.

NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity.

This study shows that CDDO-Me activates NRF2 to protect AC16 human cardiomyocytes from doxorubicin-induced toxicity by modulating p53 signaling, apoptosis, and ferroptosis.