About this Research Topic
The incidence of malignant tumors and cardiovascular diseases is on the rise all over the world, and the cases of these combined morbidities are commonly seen in clinical practice. As the survival rate of patients with malignant tumors improves, the proportion of cancer patients with cardiovascular diseases is increasing, which is also a result of the cardiovascular damage brought on by anti-tumor medication. Cardiotoxicity due to antineoplastic medicines is a significant factor influencing cardiovascular outcomes, leading to adverse cardiac remodelling and heart failure, etc.
Anthracyclines, as well-known chemotherapy medications, are frequently utilized, either alone or combined with other chemotherapeutics. DOX (also known as doxorubicin, a typical anthracycline) has been widely used for its efficacy in the treatment of tumors. Due to their non-specific cellular targets and cardiotoxicity in cardiomyocytes with dose-dependent, however, they are limited in long-term clinical application.
Oxidative stress is the currently recognized mechanism of anthracyclines causing cardiotoxicity. DOX directly induces oxidative stress. The quinone-based structure of DOX generates a large number of reactive oxygen species under the action of abundant reductases in mitochondria, thereby causing cardiomyocyte damage and apoptosis. These may interact with proteins, lipids, DNA, protein malfunction, and lipid peroxidation. The antioxidant capacity of cardiomyocytes is decreased by DOX, which decreases the expression and activity of antioxidant enzymes. Anthracyclines also chelate iron ions to form complexes, generate oxygen free radicals through redox reactions to cause cardiac injury.
The regulation of oxidative stress is a spotlight issue on cardio-oncology. We aim to focus on oxidative stress prevention, treatment, and rehabilitation approaches for cardio-oncology and associated risk factors. The potential role of redox balances in the prevention and management of cardiotoxicity caused by anti-cancer therapy are encouraged to be highlighted.
We welcome submissions on the following topics, but are not limited to:
- The mechanism of oxidative stress regulation in anti-cancer therapies-related cardiotoxicity
- Oxidative stress and apoptosis in anti-cancer therapies-related cardiotoxicity.
- Oxidative stress and stress-activated signaling pathways in antineoplastic medicines induced cardiotoxicity
- Bioactive natural compounds in treatment of antineoplastic medicines induced cardiotoxicity
- Reactive oxygen species generation and dietary management of anti-cancer therapies-related cardiotoxicity
Anthracyclines, as well-known chemotherapy medications, are frequently utilized, either alone or combined with other chemotherapeutics. DOX (also known as doxorubicin, a typical anthracycline) has been widely used for its efficacy in the treatment of tumors. Due to their non-specific cellular targets and cardiotoxicity in cardiomyocytes with dose-dependent, however, they are limited in long-term clinical application.
Oxidative stress is the currently recognized mechanism of anthracyclines causing cardiotoxicity. DOX directly induces oxidative stress. The quinone-based structure of DOX generates a large number of reactive oxygen species under the action of abundant reductases in mitochondria, thereby causing cardiomyocyte damage and apoptosis. These may interact with proteins, lipids, DNA, protein malfunction, and lipid peroxidation. The antioxidant capacity of cardiomyocytes is decreased by DOX, which decreases the expression and activity of antioxidant enzymes. Anthracyclines also chelate iron ions to form complexes, generate oxygen free radicals through redox reactions to cause cardiac injury.
The regulation of oxidative stress is a spotlight issue on cardio-oncology. We aim to focus on oxidative stress prevention, treatment, and rehabilitation approaches for cardio-oncology and associated risk factors. The potential role of redox balances in the prevention and management of cardiotoxicity caused by anti-cancer therapy are encouraged to be highlighted.
We welcome submissions on the following topics, but are not limited to:
- The mechanism of oxidative stress regulation in anti-cancer therapies-related cardiotoxicity
- Oxidative stress and apoptosis in anti-cancer therapies-related cardiotoxicity.
- Oxidative stress and stress-activated signaling pathways in antineoplastic medicines induced cardiotoxicity
- Bioactive natural compounds in treatment of antineoplastic medicines induced cardiotoxicity
- Reactive oxygen species generation and dietary management of anti-cancer therapies-related cardiotoxicity
Keywords: oxidative stress, cardio-oncology, mechanisms, prevention, treatment
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