☆ 4.6 Editorial Material

Sexual dimorphism in doxorubicin cardiotoxicity: two sides of a complex coin

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY (2023)

Anthracycline cardiotoxicity is exacerbated by global p38β genetic ablation in a sexually dimorphic manner but unaltered by cardiomyocyte-specific p38α loss

Sharon A. George et al.

Summary: This study reveals the sex- and isoform-specific roles of p38 MAPKs in DOX-induced cardiac injury. Global p38 beta deletion aggravated DIC and worsened cardiac function deterioration, while cardiomyocyte-specific p38 alpha deletion improved survival of male mice. These findings have important implications for understanding and treating DIC.

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY (2023)

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Article Cardiac & Cardiovascular Systems

Preclinical Models of Cancer Therapy-Associated Cardiovascular Toxicity: A Scientific Statement From the American Heart Association

Aarti Asnani et al.

Summary: Cardio-oncology has emerged as a new field focusing on the cardiovascular toxicity associated with cancer therapy, aiming to understand the underlying molecular mechanisms to improve patient outcomes. The intersection of cancer and heart disease has led to the discovery of genetic and environmental risk factors predisposing to both conditions. Preclinical models serve as the foundation for mechanistic studies in the development of biomarkers and cardioprotective therapies.

CIRCULATION RESEARCH (2021)

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Article Cardiac & Cardiovascular Systems

Testosterone Antagonizes Doxorubicin-Induced Senescence of Cardiomyocytes

Paola Altieri et al.

JOURNAL OF THE AMERICAN HEART ASSOCIATION (2016)

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Article Cell Biology

Reversal of Mitochondrial Transhydrogenase Causes Oxidative Stress in Heart Failure

Alexander G. Nickel et al.

CELL METABOLISM (2015)

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Review Cardiac & Cardiovascular Systems

Cancer Therapy-Induced Cardiotoxicity: Basic Mechanisms and Potential Cardioprotective Therapies

Virginia Shalkey Hahn et al.

JOURNAL OF THE AMERICAN HEART ASSOCIATION (2014)

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Sexual dimorphism in doxorubicin cardiotoxicity: two sides of a complex coin

相关参考文献

Anthracycline cardiotoxicity is exacerbated by global p38β genetic ablation in a sexually dimorphic manner but unaltered by cardiomyocyte-specific p38α loss

Preclinical Models of Cancer Therapy-Associated Cardiovascular Toxicity: A Scientific Statement From the American Heart Association

Testosterone Antagonizes Doxorubicin-Induced Senescence of Cardiomyocytes

Reversal of Mitochondrial Transhydrogenase Causes Oxidative Stress in Heart Failure

Cancer Therapy-Induced Cardiotoxicity: Basic Mechanisms and Potential Cardioprotective Therapies

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