0000000000223839

AUTHOR

Claudia Penna

showing 3 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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Sex differences in anthracycline-induced cardiotoxicity: the benefits of estrogens

2019

Anthracyclines are the cornerstone for many oncologic treatments, but their cardiotoxicity has been recognized for several decades. Female subjects, especially before puberty and adolescence, or after menopause, seem to be more at increased risk, with the prognostic impact of this sex issue being less consistent compared to other cardiovascular risk factors. Several studies imply that sex differences could depend on the lack of the protective effect of sex hormones against the anthracycline-initiated damage in cardiac cells, or on differential mitochondria-related oxidative gene expression. This is also reflected by the results obtained with different diagnostic methods, such as cardiovascu…

MaleCardiac & Cardiovascular SystemsMagnetic Resonance Spectroscopyand protection from anthracycline cardiotoxicitymedicine.disease_causeBioinformaticsRisk FactorsAnthracycline cardiotoxicityGender differenceGender differencesAnthracyclinesGonadal Steroid Hormones1102 Cardiorespiratory Medicine and HaematologyAMERICAN SOCIETYCardioprotectionSex CharacteristicsHeartPrognosisMitochondriaMenopauseEchocardiographyReperfusion InjuryHEART-FAILUREAnthracycline cardiotoxicity; Gender differences; Pathophysiology monitoring and protection from anthracycline cardiotoxicity; Anthracyclines; Biomarkers; Cardiotonic Agents; Cardiotoxicity; Echocardiography; Female; Gonadal Steroid Hormones; Heart; Heart Failure; Humans; Magnetic Resonance Spectroscopy; Male; Mitochondria; Nuclear Medicine; Oxidative Stress; Prognosis; Reperfusion Injury; Risk Factors; Sex CharacteristicsFemaleCardiology and Cardiovascular MedicineLife Sciences & BiomedicinePOSITION PAPERCARDIAC DYSFUNCTIONCardiotonic AgentsAnthracyclineSPECKLE-TRACKINGIschemiaDRUG CARDIOTOXICITYPathophysiologymedicineHumansCHILDHOOD-CANCER SURVIVORSBREAST-CANCERPathophysiology monitoring and protection from anthracycline cardiotoxicityHeart FailureCardiotoxicityScience & Technologybusiness.industryWORKING GROUPmedicine.diseaseCardiotoxicityOxidative StressmonitoringCardiovascular System & HematologyHeart failureCardiovascular System & CardiologyRISK-FACTORSNuclear MedicinebusinessOxidative stressAnthracycline cardiotoxicity; Gender differences; Pathophysiology monitoring and protection from anthracycline cardiotoxicityBiomarkersHormone
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From molecular mechanisms to clinical management of antineoplastic drug-induced cardiovascular toxicity: A translational overview

2019

Significance: Antineoplastic therapies have significantly improved the prognosis of oncology patients. However, these treatments can bring to a higher incidence of side-effects, including the worrying cardiovascular toxicity (CTX). Recent Advances: Substantial evidence indicates multiple mechanisms of CTX, with redox mechanisms playing a key role. Recent data singled out mitochondria as key targets for antineoplastic drug-induced CTX; understanding the underlying mechanisms is, therefore, crucial for effective cardioprotection, without compromising the efficacy of anti-cancer treatments. Critical Issues: CTX can occur within a few days or many years after treatment. Type I CTX is associated…

Cardiovascular toxicityPhysiologymedicine.medical_treatmentAntineoplastic drugClinical BiochemistryAntineoplastic Agents030204 cardiovascular system & hematologyPharmacologyBiochemistryCardiac cellcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factor; Antineoplastic Agents; Cardiotoxicity; Humans; Mitochondria; Oxidation-Reduction03 medical and health scienceschemistry.chemical_compoundErbB2 inhibitors cancer immunotherapy chemotherapy oxidative/nitrosative stress tyrosine kinase inhibitors vascular endothelial growth factor0302 clinical medicinetyrosine kinase inhibitorcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factorChemotherapy; ErbB2 inhibitors; vascular endothelial growth factor; tyrosine kinase inhibitors; oxidative/nitrosative stress; cancer immunotherapyCancer immunotherapytyrosine kinase inhibitorsmedicineHumansChemotherapyMolecular BiologyGeneral Environmental ScienceCardioprotectionComprehensive Invited ReviewsChemotherapyErbB2 inhibitorcancer immunotherapyvascular endothelial growth factorbusiness.industryCell BiologyCardiotoxicityMitochondriaVascular endothelial growth factoroxidative/nitrosative streErbB2 inhibitorschemistry030220 oncology & carcinogenesisGeneral Earth and Planetary SciencesbusinessOxidation-ReductionAfter treatmentoxidative/nitrosative stress
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