Anthracycline-induced cardiotoxicity: targeting high-density lipoproteins to limit the damage?

Abstract Doxorubicin (DOX) is an anthracycline antibiotic frequently used against a wide range of cancers, including breast cancer. Although the drug is effective as a treatment against cancer, many patients develop heart failure (HF) months to years following their last treatment with DOX. The chal...

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Main Authors: Carmelita Abrahams, Nicholas J. Woudberg, Sandrine Lecour
Format: Article
Language:English
Published: BMC 2022-09-01
Series:Lipids in Health and Disease
Subjects:
Online Access:https://doi.org/10.1186/s12944-022-01694-y
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author Carmelita Abrahams
Nicholas J. Woudberg
Sandrine Lecour
author_facet Carmelita Abrahams
Nicholas J. Woudberg
Sandrine Lecour
author_sort Carmelita Abrahams
collection DOAJ
description Abstract Doxorubicin (DOX) is an anthracycline antibiotic frequently used against a wide range of cancers, including breast cancer. Although the drug is effective as a treatment against cancer, many patients develop heart failure (HF) months to years following their last treatment with DOX. The challenge in preventing DOX-induced cardiotoxicity is that symptoms present after damage has already occurred in the myocardium. Therefore, early biomarkers to assess DOX-induced cardiotoxicity are urgently needed. A better understanding of the mechanisms involved in the toxicity is important as this may facilitate the development of novel early biomarkers or therapeutic approaches. In this review, we discuss the role of high-density lipoprotein (HDL) particles and its components as possible key players in the early development of DOX-induced cardiotoxicity. HDL particles exist in different subclasses which vary in composition and biological functionality. Multiple cardiovascular risk factors are associated with a change in HDL subclasses, resulting in modifications of their composition and physiological functions. There is growing evidence in the literature suggesting that cancer affects HDL subclasses and that healthy HDL particles enriched with sphingosine-1-phosphate (S1P) and apolipoprotein A1 (ApoA1) protect against DOX-induced cardiotoxicity. Here, we therefore discuss associations and relationships between HDL, DOX and cancer and discuss whether assessing HDL subclass/composition/function may be considered as a possible early biomarker to detect DOX-induced cardiotoxicity.
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spelling doaj.art-33bda5b623c74f33a0279152870402792022-12-22T03:12:24ZengBMCLipids in Health and Disease1476-511X2022-09-0121111610.1186/s12944-022-01694-yAnthracycline-induced cardiotoxicity: targeting high-density lipoproteins to limit the damage?Carmelita Abrahams0Nicholas J. Woudberg1Sandrine Lecour2Cardioprotection Group, Cape Heart Institute and Hatter Institute for Cardiovascular Research in Africa, Department of Medicine, Faculty of Health Sciences, University of Cape TownCardioprotection Group, Cape Heart Institute and Hatter Institute for Cardiovascular Research in Africa, Department of Medicine, Faculty of Health Sciences, University of Cape TownCardioprotection Group, Cape Heart Institute and Hatter Institute for Cardiovascular Research in Africa, Department of Medicine, Faculty of Health Sciences, University of Cape TownAbstract Doxorubicin (DOX) is an anthracycline antibiotic frequently used against a wide range of cancers, including breast cancer. Although the drug is effective as a treatment against cancer, many patients develop heart failure (HF) months to years following their last treatment with DOX. The challenge in preventing DOX-induced cardiotoxicity is that symptoms present after damage has already occurred in the myocardium. Therefore, early biomarkers to assess DOX-induced cardiotoxicity are urgently needed. A better understanding of the mechanisms involved in the toxicity is important as this may facilitate the development of novel early biomarkers or therapeutic approaches. In this review, we discuss the role of high-density lipoprotein (HDL) particles and its components as possible key players in the early development of DOX-induced cardiotoxicity. HDL particles exist in different subclasses which vary in composition and biological functionality. Multiple cardiovascular risk factors are associated with a change in HDL subclasses, resulting in modifications of their composition and physiological functions. There is growing evidence in the literature suggesting that cancer affects HDL subclasses and that healthy HDL particles enriched with sphingosine-1-phosphate (S1P) and apolipoprotein A1 (ApoA1) protect against DOX-induced cardiotoxicity. Here, we therefore discuss associations and relationships between HDL, DOX and cancer and discuss whether assessing HDL subclass/composition/function may be considered as a possible early biomarker to detect DOX-induced cardiotoxicity.https://doi.org/10.1186/s12944-022-01694-yCardio-oncologyAnthracyclineHigh-density lipoproteinsCardiac toxicity
spellingShingle Carmelita Abrahams
Nicholas J. Woudberg
Sandrine Lecour
Anthracycline-induced cardiotoxicity: targeting high-density lipoproteins to limit the damage?
Lipids in Health and Disease
Cardio-oncology
Anthracycline
High-density lipoproteins
Cardiac toxicity
title Anthracycline-induced cardiotoxicity: targeting high-density lipoproteins to limit the damage?
title_full Anthracycline-induced cardiotoxicity: targeting high-density lipoproteins to limit the damage?
title_fullStr Anthracycline-induced cardiotoxicity: targeting high-density lipoproteins to limit the damage?
title_full_unstemmed Anthracycline-induced cardiotoxicity: targeting high-density lipoproteins to limit the damage?
title_short Anthracycline-induced cardiotoxicity: targeting high-density lipoproteins to limit the damage?
title_sort anthracycline induced cardiotoxicity targeting high density lipoproteins to limit the damage
topic Cardio-oncology
Anthracycline
High-density lipoproteins
Cardiac toxicity
url https://doi.org/10.1186/s12944-022-01694-y
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AT nicholasjwoudberg anthracyclineinducedcardiotoxicitytargetinghighdensitylipoproteinstolimitthedamage
AT sandrinelecour anthracyclineinducedcardiotoxicitytargetinghighdensitylipoproteinstolimitthedamage