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Molecular Mechanisms of Myocardial Injury and Ventricular Dysfunction: Pathways and...
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Molecular Mechanisms of Myocardial Injury and Ventricular Dysfunction: Pathways and Therapeutic Targets

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 December 2025 | Viewed by 148

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,

This Special Issue aims to gather the latest research focusing on the molecular and cellular mechanisms underlying myocardial injury and ventricular dysfunction. The objectives include:

To elucidate key signaling pathways involved in cardiac injury and remodeling, such as oxidative stress, inflammation, apoptosis, and fibrosis;  To explore novel molecular targets and biomarkers for early diagnosis and prognosis of ventricular dysfunction; To highlight advances in pharmacological and genetic interventions that mitigate myocardial damage and improve cardiac function; To foster interdisciplinary approaches integrating molecular biology, pharmacology, and clinical insights to better understand cardiac pathophysiology.

We welcome original research articles, comprehensive reviews, and translational studies that deepen understanding of myocardial injury at the molecular level and its impact on ventricular function. Contributions investigating new therapeutic strategies, including drug development, gene therapy, and molecular modulators, are especially encouraged.

Dr. Antonio Lax
Guest Editor

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

  • myocardial injury
  • ventricular dysfunction
  • drug development
  • gene therapy
  • molecular modulators

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Published Papers (1 paper)

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Review

24 pages, 2744 KB  
Review
miR-106b-5p as a Central Regulator of Cancer Progression and Chemotherapy-Induced Cardiotoxicity: From Molecular Mechanisms to Clinical Translation
by Maria del Carmen Asensio Lopez, Miriam Ruiz Ballester, Francisco Jose Bastida Nicolas, Fernando Soler Pardo, Jose Luis Alonso-Romero, Cesar Caro-Martinez, Domingo Pascual Figal and Antonio Lax
Int. J. Mol. Sci. 2025, 26(20), 10002; https://doi.org/10.3390/ijms262010002 - 14 Oct 2025
Abstract
MicroRNAs (miRNAs) are critical regulators of gene expression in cancer biology and cardiovascular disease. miR-106b-5p, a member of the miR-106b-25 cluster, has been widely studied for its oncogenic activity in various malignancies. However, its role as a direct molecular driver of anthracycline-induced cardiotoxicity [...] Read more.
MicroRNAs (miRNAs) are critical regulators of gene expression in cancer biology and cardiovascular disease. miR-106b-5p, a member of the miR-106b-25 cluster, has been widely studied for its oncogenic activity in various malignancies. However, its role as a direct molecular driver of anthracycline-induced cardiotoxicity has only recently been uncovered. This finding highlights new therapeutic possibilities at the intersection of oncology and cardiovascular medicine. This review outlines the dual role of miR-106b-5p as a key modulator in both tumor progression and chemotherapy-induced cardiac dysfunction. miR-106b-5p is upregulated in numerous cancers—including breast, prostate, lung, gastric, colorectal, hepatocellular, and esophageal—and promotes tumorigenesis via suppression of tumor suppressors such as PTEN, BTG3, p21, and SMAD7, leading to activation of oncogenic pathways like PI3K/AKT and TGF-β. Importantly, we present the first evidence that miR-106b-5p is significantly upregulated in the myocardium in response to doxorubicin treatment, where it drives left ventricular dysfunction by targeting PR55α, a key regulator of PP2A activity. This pathway results in cytoplasmic HDAC4 accumulation, aberrant activation of the YY1 transcription factor, and upregulation of sST2, a biomarker linked to adverse cardiac remodeling and poor prognosis. In response, we developed AM106, a novel locked nucleic acid antagomir that silences miR-106 b-5p. Preclinical studies demonstrate that AM106 restores PR55α/PP2A activity, reduces sST2 expression, and prevents structural and functional cardiac damage without compromising anti-tumor efficacy. In parallel, artificial intelligence (AI) tools could be leveraged in the future—based on established AI applications in miRNA cancer research—to accelerate the identification of miR-106b-5p-related biomarkers and guide personalized therapy selection. Our findings position miR-106b-5p as a previously unrecognized molecular bridge between cancer and doxorubicin-induced cardiotoxicity. The development of the AM106 antagomir represents a promising approach with potential clinical applicability in cardio-oncology, offering dual benefits: tumor control and cardioprotection. Coupling this innovation with AI-driven analysis of patient data may enable precision risk stratification, early intervention, and improved outcomes. miR-106b-5p thus emerges as a central therapeutic target and biomarker candidate for transforming the clinical management of cancer patients at risk for heart failure. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Myocardial Injury and Ventricular Dysfunction: Pathways and Therapeutic Targets)
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