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Molecular Target for Cardioprotection and Cardiotoxicity

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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 (15 November 2022) | Viewed by 10313

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Special Issue Editors

Prof. Dr. Ioanna Andreadou

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Laboratory of Pharmacology, Faculty of Pharmacy, National and Kapodistrian University of Athens, Athens, Greece
Interests: cardiovascular pharmacology; cardioprotection; oxidative stress; molecular toxicology
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Rainer Schulz

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Department of Physiology, University of Giessen, 35392 Giessen, Germany
Interests: ischemia; reperfusion; heart; cardioprotection; mitochondria; signalling
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Prof. Dr. Péter Ferdinandy

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Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary
Interests: cardioprotection; cardiotoxicity; metabolic comorbidities; transcriptomics; network medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ischemic heart disease (IHD) is a leading cause of death and disability worldwide. Despite intensive experimental research over the last three to four decades, there is currently no effective therapy for protecting the heart against failure following acute myocardial infarction—also termed cardioprotection. Therefore, novel molecular targets for cardioprotection need to be discovered in order to improve the clinical outcomes of IHD patients. This is the overall objective of our EU-CARDIOPROTECTION COST Action (CA16225 http://www.cardioprotection.eu/), which comprises a European network of 100 leading cardioprotection researchers, dedicated to realizing the therapeutic potential of novel cardioprotective therapies for the benefit of patients. This will be achieved through the discovery of novel therapeutic targets and strategies for cardioprotection (such as combination multitargeted therapies) as well as investigations into the confounding effects of co-morbidities and co-medication on cardioprotection.

For the latter, cancer and cancer therapy play an important role. The cardiotoxicity induced by chemotherapy is a life-threatening consequence that limits the use of several chemotherapy drugs in clinical practice. Myocardial ischemia, heart failure, and arrhythmias leading to sudden cardiac death are the most feared complications of chemotherapy. Although various pathophysiological mechanisms have been proposed that underlie the ischemic complications of anticancer drugs, cancer-therapy-related cardiotoxicity remains a major challenge, and the recognition of novel targets for the management of the cardiotoxicity of the various chemotherapeutic agents is essential.

Therefore, in this Special Issue on “Molecular Target for Cardioprotection and Cardiotoxicity" of IJMS, we invite you to submit both review and original preclinical articles on the topic of cardioprotection and cardiotoxicity, with a special focus on novel molecular targets.

Prof. Dr. Ioanna Andreadou
Prof. Dr. Rainer Schulz
Prof. Dr. Péter Ferdinandy
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

cardioprotection
cardiotoxicity
cardiovascular pharmacology

Published Papers (4 papers)

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Research

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12 pages, 2013 KiB

Open AccessArticle

Effects of Bempedoic Acid in Acute Myocardial Infarction in Rats: No Cardioprotection and No Hidden Cardiotoxicity

by Tamás G. Gergely, Gábor B. Brenner, Regina N. Nagy, Nabil V. Sayour, András Makkos, Csenger Kovácsházi, Huimin Tian, Rainer Schulz, Zoltán Giricz, Anikó Görbe and Péter Ferdinandy

Int. J. Mol. Sci. 2023, 24(2), 1585; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24021585 - 13 Jan 2023

Viewed by 1557

Abstract

Lipid-lowering drugs have been shown to have cardioprotective effects but may have hidden cardiotoxic properties. Therefore, here we aimed to investigate if chronic treatment with the novel lipid-lowering drug bempedoic acid (BA) exerts hidden cardiotoxic and/or cardioprotective effects in a rat model of acute myocardial infarction (AMI). Wistar rats were orally treated with BA or its vehicle for 28 days, anesthetized and randomized to three different groups (vehicle + ischemia/reperfusion (I/R), BA + I/R, and positive control vehicle + ischemic preconditioning (IPC)) and subjected to cardiac 30 min ischemia and 120 min reperfusion. IPC was performed by 3 × 5 min I/R cycles before ischemia. Myocardial function, area at risk, infarct size and arrhythmias were analyzed. Chronic BA pretreatment did not influence cardiac function or infarct size as compared to the vehicle group, while the positive control IPC significantly reduced the infarct size. The incidence of reperfusion-induced arrhythmias was significantly reduced by BA and IPC. This is the first demonstration that BA treatment does not show cardioprotective effect although moderately reduces the incidence of reperfusion-induced arrhythmias. Furthermore, BA does not show hidden cardiotoxic effect in rats with AMI, showing its safety in the ischemic/reperfused heart. Full article

(This article belongs to the Special Issue Molecular Target for Cardioprotection and Cardiotoxicity)

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13 pages, 1423 KiB

Open AccessArticle

Trastuzumab and Doxorubicin Sequential Administration Increases Oxidative Stress and Phosphorylation of Connexin 43 on Ser368

by Michela Pecoraro, Stefania Marzocco, Silvia Franceschelli and Ada Popolo

Int. J. Mol. Sci. 2022, 23(12), 6375; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23126375 - 07 Jun 2022

Cited by 4 | Viewed by 1827

Abstract

Human epidermal growth factor receptor-2 (HER2) is overexpressed in up to 30% of breast cancer cases, causing a more aggressive tumour growth and poor prognosis. Trastuzumab, the humanized antibody targeted to HER2, increased the life expectancy of patients, but severe cardiotoxicity emerged as a long-term adverse effect. Clinical evidence highlights that Trastuzumab-induced cardiotoxicity drastically increases in association with Doxorubicin; however, the exact mechanisms involved remain incompletely understood. In order to analyse the molecular mechanisms involved and the possible adaptative responses to Trastuzumab and Doxorubicin treatment, in this study, H9c2 cardiomyoblasts were used. Results showed that Trastuzumab and Doxorubicin sequential administration in cardiomyoblast increased cytosolic and mitochondrial ROS production, intracellular calcium dysregulation, mitochondrial membrane depolarization, and the consequent apoptosis, induced by both Trastuzumab and Doxorubicin alone. Furthermore, in these conditions, we observed increased levels of Connexin43 phosphorylated on Ser368 (pCx43). Since phosphorylation on Ser368 decreases gap junction intracellular communication, thus reducing the spread of death signals to adjacent cells, we hypothesized that the increase in pCx43 could be an adaptative response implemented by cells to defend neighbouring cells by Trastuzumab and Doxorubicin sequential administration. However, the other side of the coin is the resulting conduction abnormalities. Full article

(This article belongs to the Special Issue Molecular Target for Cardioprotection and Cardiotoxicity)

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Review

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39 pages, 2340 KiB

Open AccessReview

Myocardial Protection and Current Cancer Therapy: Two Opposite Targets with Inevitable Cost

by Panagiotis Efentakis, Ioanna Andreadou, Konstantinos E. Iliodromitis, Filippos Triposkiadis, Péter Ferdinandy, Rainer Schulz and Efstathios K. Iliodromitis

Int. J. Mol. Sci. 2022, 23(22), 14121; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232214121 - 15 Nov 2022

Cited by 4 | Viewed by 2348

Abstract

Myocardial protection against ischemia/reperfusion injury (IRI) is mediated by various ligands, activating different cellular signaling cascades. These include classical cytosolic mediators such as cyclic-GMP (c-GMP), various kinases such as Phosphatydilinositol-3- (PI3K), Protein Kinase B (Akt), Mitogen-Activated-Protein- (MAPK) and AMP-activated (AMPK) kinases, transcription factors such as signal transducer and activator of transcription 3 (STAT3) and bioactive molecules such as vascular endothelial growth factor (VEGF). Most of the aforementioned signaling molecules constitute targets of anticancer therapy; as they are also involved in carcinogenesis, most of the current anti-neoplastic drugs lead to concomitant weakening or even complete abrogation of myocardial cell tolerance to ischemic or oxidative stress. Furthermore, many anti-neoplastic drugs may directly induce cardiotoxicity via their pharmacological effects, or indirectly via their cardiovascular side effects. The combination of direct drug cardiotoxicity, indirect cardiovascular side effects and neutralization of the cardioprotective defense mechanisms of the heart by prolonged cancer treatment may induce long-term ventricular dysfunction, or even clinically manifested heart failure. We present a narrative review of three therapeutic interventions, namely VEGF, proteasome and Immune Checkpoint inhibitors, having opposing effects on the same intracellular signal cascades thereby affecting the heart. Moreover, we herein comment on the current guidelines for managing cardiotoxicity in the clinical setting and on the role of cardiovascular confounders in cardiotoxicity. Full article

(This article belongs to the Special Issue Molecular Target for Cardioprotection and Cardiotoxicity)

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40 pages, 3638 KiB

Open AccessReview

Cardio-Oncology: Mechanisms, Drug Combinations, and Reverse Cardio-Oncology

by Zehua Liang, Yuquan He and Xin Hu

Int. J. Mol. Sci. 2022, 23(18), 10617; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231810617 - 13 Sep 2022

Cited by 20 | Viewed by 3897

Abstract

Chemotherapy, radiotherapy, targeted therapy, and immunotherapy have brought hope to cancer patients. With the prolongation of survival of cancer patients and increased clinical experience, cancer-therapy-induced cardiovascular toxicity has attracted attention. The adverse effects of cancer therapy that can lead to life-threatening or induce long-term morbidity require rational approaches to prevention and treatment, which requires deeper understanding of the molecular biology underpinning the disease. In addition to the drugs used widely for cardio-protection, traditional Chinese medicine (TCM) formulations are also efficacious and can be expected to achieve “personalized treatment” from multiple perspectives. Moreover, the increased prevalence of cancer in patients with cardiovascular disease has spurred the development of “reverse cardio-oncology”, which underscores the urgency of collaboration between cardiologists and oncologists. This review summarizes the mechanisms by which cancer therapy induces cardiovascular toxicity, the combination of antineoplastic and cardioprotective drugs, and recent advances in reverse cardio-oncology. Full article

(This article belongs to the Special Issue Molecular Target for Cardioprotection and Cardiotoxicity)

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