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 cardiovascular biomarkers and imaging techniques (echocardiography, magnetic resonance, and nuclear medicine) in the diagnosis and monitoring of cardiotoxicity, confirming that sex differences exist. The same is true about protective strategies from anthracycline cardiotoxicity. Indeed, first studied to withstand oxidative damage in response to ischemia/reperfusion (I/R) injury, cardioprotection has different outcomes in men and women. A number of studies assessed the differences in I/R response between male and female hearts, with oxidative stress and apoptosis being shared mechanisms between the I/R and anthracyclines heart damage. Sex hormones can modulate these mechanisms, thus confirming their importance in the pathophysiology in cardioprotection not only from the ischemia/reperfusion damage, but also from anthracyclines, fueling further cardio-oncologic research on the topic.

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

Penna C.
Co-first
;
2019-01-01

Abstract

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 cardiovascular biomarkers and imaging techniques (echocardiography, magnetic resonance, and nuclear medicine) in the diagnosis and monitoring of cardiotoxicity, confirming that sex differences exist. The same is true about protective strategies from anthracycline cardiotoxicity. Indeed, first studied to withstand oxidative damage in response to ischemia/reperfusion (I/R) injury, cardioprotection has different outcomes in men and women. A number of studies assessed the differences in I/R response between male and female hearts, with oxidative stress and apoptosis being shared mechanisms between the I/R and anthracyclines heart damage. Sex hormones can modulate these mechanisms, thus confirming their importance in the pathophysiology in cardioprotection not only from the ischemia/reperfusion damage, but also from anthracyclines, fueling further cardio-oncologic research on the topic.
2019
24
6
915
925
Anthracycline cardiotoxicity; Gender differences; Pathophysiology, monitoring, and protection from anthracycline cardiotoxicity
Cadeddu Dessalvi C.; Pepe A.; Penna C.; Gimelli A.; Madonna R.; Mele D.; Monte I.; Novo G.; Nugara C.; Zito C.; Moslehi J.J.; de Boer R.A.; Lyon A.R.; Tocchetti C.G.; Mercuro G.
File in questo prodotto:
File Dimensione Formato  
Gender.pdf

Accesso aperto

Descrizione: articolo principale
Tipo di file: POSTPRINT (VERSIONE FINALE DELL’AUTORE)
Dimensione 517.23 kB
Formato Adobe PDF
517.23 kB Adobe PDF Visualizza/Apri
Penna Claudia_R1_422849_Sex differences.pdf

Accesso riservato

Tipo di file: PDF EDITORIALE
Dimensione 565.46 kB
Formato Adobe PDF
565.46 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/1736812
Citazioni
  • ???jsp.display-item.citation.pmc??? 23
  • Scopus 31
  • ???jsp.display-item.citation.isi??? 32
social impact