» Articles » PMID: 39249555

Cardioprotection Strategies for Anthracycline Cardiotoxicity

Overview
Date 2024 Sep 9
PMID 39249555
Authors
Affiliations
Soon will be listed here.
Abstract

Thanks to the fantastic progress in cancer therapy options, there is a growing population of cancer survivors. This success has resulted in a need to focus much effort into improving the quality of life of this population. Cancer and cardiovascular disease share many common risk factors and have an interplay between them, with one condition mechanistically affecting the other and vice versa. Furthermore, widely prescribed cancer therapies have known toxic effects in the cardiovascular system. Anthracyclines are the paradigm of efficacious cancer therapy widely prescribed with a strong cardiotoxic potential. While some cancer therapies cardiovascular toxicities are transient, others are irreversible. There is a growing need to develop cardioprotective therapies that, when used in conjunction with cancer therapies, can prevent cardiovascular toxicity and thus improve long-term quality of life in survivors. The field has three main challenges: (i) identification of the ultimate mechanisms leading to cardiotoxicity to (ii) identify specific therapeutic targets, and (iii) more sensible diagnostic tools to early identify these conditions. In this review we will focus on the cardioprotective strategies tested and under investigation. We will focus this article into anthracycline cardiotoxicity since it is still the agent most widely prescribed, the one with higher toxic effects on the heart, and the most widely studied.

Citing Articles

SGLT2i Therapy Prevents Anthracycline-Induced Cardiotoxicity in a Large Animal Model by Preserving Myocardial Energetics.

Medina-Hernandez D, Cadiz L, Mastrangelo A, Moreno-Arciniegas A, Fernandez Tocino M, Cueto Becerra A JACC CardioOncol. 2025; 7(2):171-184.

PMID: 39967204 PMC: 11866421. DOI: 10.1016/j.jaccao.2024.12.004.


Inter-organ communication: pathways and targets to cardioprotection and neuro-protection. A report from the 12th Hatter Cardiovascular Institute workshop.

Pearce L, Galan-Arriola C, Bell R, Carr R, Cunningham J, Davidson S Basic Res Cardiol. 2024; .

PMID: 39681732 DOI: 10.1007/s00395-024-01094-6.


The cardio-oncologic burden of breast cancer: molecular mechanisms and importance of preclinical models.

Brauer J, Tumani M, Frey N, Lehmann L Basic Res Cardiol. 2024; 120(1):91-112.

PMID: 39621070 PMC: 11790711. DOI: 10.1007/s00395-024-01090-w.

References
1.
Pakravan G, Peymani M, Abedpoor N, Safaeinejad Z, Yadegari M, Derakhshan M . Antiapoptotic and anti-inflammatory effects of Pparγ agonist, pioglitazone, reversed Dox-induced cardiotoxicity through mediating of miR-130a downregulation in C57BL/6 mice. J Biochem Mol Toxicol. 2022; 36(6):e23041. DOI: 10.1002/jbt.23041. View

2.
Li H, Cheng Z, Fu X, Liu M, Liu P, Cao W . Decoding acute myocarditis in patients with COVID-19: Early detection through machine learning and hematological indices. iScience. 2024; 27(2):108524. PMC: 10831249. DOI: 10.1016/j.isci.2023.108524. View

2.
Kleinbongard P, Andreadou I . Is There a Mitochondrial Protection via Remote Ischemic Conditioning in Settings of Anticancer Therapy Cardiotoxicity?. Curr Heart Fail Rep. 2024; 21(4):292-304. PMC: 11333552. DOI: 10.1007/s11897-024-00658-w. View

3.
Furihata T, Maekawa S, Takada S, Kakutani N, Nambu H, Shirakawa R . Premedication with pioglitazone prevents doxorubicin-induced left ventricular dysfunction in mice. BMC Pharmacol Toxicol. 2021; 22(1):27. PMC: 8103594. DOI: 10.1186/s40360-021-00495-w. View

4.
Aratani Y . Myeloperoxidase: Its role for host defense, inflammation, and neutrophil function. Arch Biochem Biophys. 2018; 640:47-52. DOI: 10.1016/j.abb.2018.01.004. View