0000000000223840

AUTHOR

Pietro Ameri

0000-0001-7167-7287

showing 2 related works from this author

Redox imbalances in ageing and metabolic alterations: Implications in cancer and cardiac diseases. An overview from the working group of cardiotoxici…

2020

Metabolic syndrome (MetS) is a well established risk factor for cardiovascular (CV) diseases. In addition, several studies indicate that MetS correlates with the increased risk of cancer in adults. The mechanisms linking MetS and cancer are not fully understood. Several risk factors involved in MetS are also cancer risk factors, such as the consumption of high calorie-food or high fat intake, low fibre intake, and sedentary lifestyle. Other common aspects of both cancer and MetS are oxidative stress and inflammation. In addition, some anticancer treatments can induce cardiotoxicity, including, for instance, left ventricular (LV) dysfunction and heart failure (HF), endothelial dysfunction an…

Oncologymedicine.medical_specialtyPhysiologyClinical BiochemistryReview030204 cardiovascular system & hematologymedicine.disease_causeBiochemistry03 medical and health sciences0302 clinical medicineInternal medicineAgeing; Cancer; Cardiovascular disease; Cardiovascular toxicity from anticancer drugs; Metabolic syndromemedicineEndothelial dysfunctionRisk factorMolecular BiologySedentary lifestyleCancerCardiotoxicitybusiness.industrylcsh:RM1-950CancerCell Biologymedicine.diseaseCardiovascular diseaseMetabolic syndromeAgeingCardiovascular toxicity from anticancer drugslcsh:Therapeutics. PharmacologyCardiovascular toxicity from anticancer drug030220 oncology & carcinogenesisHeart failureMetabolic syndromebusinessOxidative stress
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Antineoplastic Drug-Induced Cardiotoxicity: A Redox Perspective

2018

Antineoplastic drugs can be associated with several side effects, including cardiovascular toxicity (CTX). Biochemical studies have identified multiple mechanisms of CTX. Chemoterapeutic agents can alter redox homeostasis by increasing the production of reactive oxygen species (ROS) and reactive nitrogen species RNS. Cellular sources of ROS/RNS are cardiomyocytes, endothelial cells, stromal and inflammatory cells in the heart. Mitochondria, peroxisomes and other subcellular components are central hubs that control redox homeostasis. Mitochondria are central targets for antineoplastic drug-induced CTX. Understanding the mechanisms of CTX is fundamental for effective cardioprotection, without…

Stromal cellPhysiologymedicine.medical_treatmentTyrosine kinase inhibitorChemotherapy; HER-2 inhibitors; Oxidative/nitrosative stress; Tyrosine kinase inhibitors; Vascular endothelial growth factorReviewOxidative phosphorylation030204 cardiovascular system & hematologyMitochondrionPharmacologyChemotherapy; HER-2 inhibitors; Oxidative/nitrosative stress; Tyrosine kinase inhibitors; Vascular endothelial growth factor; Physiology; Physiology (medical)chemotherapyHER-2 inhibitorlcsh:Physiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysiology (medical)tyrosine kinase inhibitorsMedicinechemotherapy HER-2 inhibitors oxidative/nitrosative stress vascular endothelial growth factor tyrosine kinase inhibitorsReactive nitrogen specieschemistry.chemical_classificationCardioprotectionReactive oxygen speciesChemotherapyCardiotoxicitylcsh:QP1-981vascular endothelial growth factorbusiness.industryOxidative/nitrosative strechemistry030220 oncology & carcinogenesisbusinessHER-2 inhibitorsoxidative/nitrosative stress
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