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Molecular Mechanisms of Cardiotoxicity
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Molecular Mechanisms of Cardiotoxicity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 3590

Special Issue Editor

Dr. Antonio Lax

E-Mail Website
Guest Editor
Department of Medicine, University of Murcia, 30120 Murcia, Spain
Interests: myocardial infarction; adverse remodeling; heart failure; cardiotoxicity; cardiac dysfunction; ventricular remodeling; cardioprotection; ischemic heart disease; cardiomyopathy; cardiac regeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiotoxicity is heart damage that arises from certain cancer treatments or drugs. It can develop years after cancer treatment. Although the molecular mechanism related to chemotherapy-induced cardiotoxicity is associated with activation of oxidative stress in oncologic patients, studies with a more standardized design and better characterized populations are necessary to evaluate novel molecular axes. Further, the development of new technologies allows the analysis of a large volume of data, which may lead to enabling a more precise description of the molecular processes related to cardiotoxicity after chemotherapy.

Here, I propose an ambitious special issue to change the conceptual framework used for the management of cardiotoxicity. The aim will be to detail novel molecular mechanisms related to cardiotoxicity, with novel pharmacological targets described to design pioneering therapies to treat or prevent cardiotoxicity related to chemotherapeutic treatments.

Dr. Antonio Lax
Guest Editor

Manuscript Submission Information

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Keywords

  • cardiac dysfunction
  • cardiotoxicity
  • atrophy
  • antagomiR
  • AAV
  • gene therapy
  • heart failure
  • oxidative stress
  • apoptosis
  • myocardial remodeling

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Published Papers (2 papers)

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27 pages, 20721 KiB  
Article
Doxorubicin-Induced Cardiotoxicity Through SIRT1 Loss Potentiates Overproduction of Exosomes in Cardiomyocytes
by Shuai Zhang, Yu Yang, Xinchen Lv, Xue Zhou, Wangqian Zhao, Linfeng Meng, Hongfei Xu, Shaohua Zhu and Ying Wang
Int. J. Mol. Sci. 2024, 25(22), 12376; https://doi.org/10.3390/ijms252212376 - 18 Nov 2024
Viewed by 1678
Abstract
Mutual interaction between doxorubicin (DOX) and cardiomyocytes is crucial for cardiotoxicity progression. Cardiomyocyte injury is an important pathological feature of DOX-induced cardiomyopathy, and its molecular pathogenesis is multifaceted. In addition to the direct toxic effects of DOX on cardiomyocytes, DOX-induced exosomes in the [...] Read more.
Mutual interaction between doxorubicin (DOX) and cardiomyocytes is crucial for cardiotoxicity progression. Cardiomyocyte injury is an important pathological feature of DOX-induced cardiomyopathy, and its molecular pathogenesis is multifaceted. In addition to the direct toxic effects of DOX on cardiomyocytes, DOX-induced exosomes in the extracellular microenvironment also regulate the pathophysiological states of cardiomyocytes. However, the mechanisms by which DOX regulates exosome secretion and subsequent pathogenesis remain incompletely understood. Here, we found that DOX significantly increased exosome secretion from cardiomyocytes, and inhibiting this release could alleviate cardiomyocyte injury. DOX promoted exosome secretion by reducing cardiomyocyte silencing information regulator 1 (SIRT1) expression, exacerbating cardiotoxicity. DOX impaired lysosomal acidification in cardiomyocytes, reducing the degradation of intracellular multivesicular bodies (MVBs), resulting in an increase in MVB volume before fusing with the plasma membrane to release their contents. Mechanistically, SIRT1 loss inhibited lysosomal acidification by reducing the expression of the ATP6V1A subunit of the lysosomal vacuolar-type H+ ATPase (V-ATPase) proton pump. Overexpressing SIRT1 increased ATP6V1A expression, improved lysosomal acidification, inhibited exosome secretion, and thereby alleviated DOX-induced cardiotoxicity. Interestingly, DOX also induced mitochondrial-derived vesicle formation in cardiomyocytes, which may further increase the abundance of MVBs and promote exosome release. Collectively, this study identified SIRT1-mediated impairment of lysosomal acidification as a key mechanism underlying the increased exosome secretion from cardiomyocytes induced by DOX, providing new insights into DOX-induced cardiotoxicity pathogenesis. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cardiotoxicity)
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Review

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21 pages, 2045 KiB  
Review
Evolution of Theories on Doxorubicin-Induced Late Cardiotoxicity-Role of Topoisomerase
by Jaroslaw Szponar, Erwin Ciechanski, Magda Ciechanska, Jaroslaw Dudka and Sławomir Mandziuk
Int. J. Mol. Sci. 2024, 25(24), 13567; https://doi.org/10.3390/ijms252413567 - 18 Dec 2024
Cited by 2 | Viewed by 1487
Abstract
Doxorubicin (DOX) has been widely used as a cytotoxic chemotherapeutic. However, DOX has a number of side effects, such as myelotoxicity or gonadotoxicity, the most dangerous of which is cardiotoxicity. Cardiotoxicity can manifest as cardiac arrhythmias, myocarditis, and pericarditis; life-threatening late cardiotoxicity can [...] Read more.
Doxorubicin (DOX) has been widely used as a cytotoxic chemotherapeutic. However, DOX has a number of side effects, such as myelotoxicity or gonadotoxicity, the most dangerous of which is cardiotoxicity. Cardiotoxicity can manifest as cardiac arrhythmias, myocarditis, and pericarditis; life-threatening late cardiotoxicity can result in heart failure months or years after the completion of chemotherapy. The development of late cardiomyopathy is not yet fully understood. The most important question is how DOX reprograms the cardiomyocyte, after which DOX is excreted from the body, initially without symptoms. However, clinically overt cardiomyopathy develops over the following months and years. Since the 1980s, DOX-induced disorders in cardiomyocytes have been thought to be related to oxidative stress and dependent on the Fe/reactive oxygen species (ROS) mechanism. That line of evidence was supported by dexrazoxane (DEX) protection, the only Food and Drug Administration (FDA)-approved drug for preventing DOX-induced cardiomyopathy, which complexes iron. Thus, the hypothesis related to Fe/ROS provides a plausible explanation for the induction of the development of late cardiomyopathy via DOX. However, in subsequent studies, DEX was used to identify another important mechanism in DOX-induced cardiomyopathy that is related to topoisomerase 2β (Top2β). Does the Top2β hypothesis explain the mechanisms of the development of DOX-dependent late heart failure? Several of these mechanisms have been identified to date, proving the involvement of Top2β in the regulation of the redox balance, including oxidative stress. Thus, the development of late cardiomyopathy can be explained based on mechanisms related to Top2β. In this review, we highlight free radical theory, iron imbalance, calcium overload, and finally, a theory based on Top2β. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cardiotoxicity)
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