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Cardioimmunology: Inflammation and Immunity in Cardiovascular Disease—2nd Edition
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Cardioimmunology: Inflammation and Immunity in Cardiovascular Disease—2nd Edition

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

Deadline for manuscript submissions: 30 September 2026 | Viewed by 442

Special Issue Editor

Dr. David Rohde

E-Mail Website1 Website2
Guest Editor
Department of Internal Medicine I and Comprehensive Heart Failure Center (CHFC), University Hospital Würzburg, Würzburg, Germany
Interests: myocardial infarction; heart failure; atherosclerosis; arterial hypertension; bone marrow; hematopoiesis; emergency myelopoiesis; endothelial cells; megakaryocytes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This is a continuation of our series on the hot topic of “Cardioimmunology: Inflammation and Immunity in Cardiovascular Disease”. We have already have published a successful Special Issue, which received interesting contributions and spurred lively discussion (https://www.mdpi.com/journal/ijms/special_issues/cardioimmunology).

Peter Libby once told me how, when he was an aspiring junior researcher, he got side-eyed by his peers for calling atherosclerosis an inflammatory disease. At that time, the interdisciplinary approach to deciphering the intricate interplay between cardiovascular tissue, inflammation, and immunity—today known as cardioimmunology—was seen as a niche area investigating a “byproduct” of blood vessel occlusion, genetic predisposition, and lifestyle factors.

A few decades later, the interaction between the immune system and cardiovascular organs has unequivocally been recognized as a driving force behind the development and progression of cardiovascular disease. By revealing the contribution of inflammation and immune cells to disease initiation and progression, cardioimmunology has reshaped our current understanding of myocardial infarction, myocarditis, atherosclerosis, heart failure, arterial hypertension, and—most recently—cardiac arrhythmia. Further insights into the molecular and cellular mechanisms of both innate and adaptive immune cell involvement offer promising avenues for novel diagnostics and targeted therapies aimed at refined prevention and improved treatment for patients suffering from cardiovascular disease.

This Special Issue seeks to capture cutting-edge research and provide expert reviews on cardioimmune interactions. We invite submissions of original research articles and comprehensive reviews that focus on a deeper understanding of how inflammation and immunity contribute to the pathogenesis, diagnosis, and treatment of cardiovascular disease.

Dr. David Rohde
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 250 words) can be sent to the Editorial Office for assessment.

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 infarction
  • heart failure
  • atherosclerosis
  • arterial hypertension
  • myocarditis
  • arrhythmia
  • inflammation
  • hematopoiesis
  • myelopoiesis
  • tissue macrophages
  • neutrophil biology
  • lymphocytes
  • endothelial cells
  • megakaryocytes
  • platelet biology
  • biomarkers

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Published Papers (1 paper)

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Review

24 pages, 1918 KB  
Review
Heart-Type Fatty Acid-Binding Protein (H-FABP) as a Candidate Adjunctive Biomarker for Immune Checkpoint Inhibitor-Related Cardiotoxicity: Linking Early Immune–Metabolic Myocardial Injury with Translational Cardio-Oncology
by Vincenzo Quagliariello, Massimiliano Berretta, Fabrizio Maurea, Maria Laura Canale, Andrea Paccone, Irma Bisceglia, Andrea Tedeschi, Marino Scherillo, Jacopo Santagata, Stefano Oliva, Christian Cadeddu Dessalvi, Pietro Forte, Cristiana D’Ambrosio, Tiziana Di Matola, Domenico Gabrielli and Nicola Maurea
Int. J. Mol. Sci. 2026, 27(11), 4842; https://doi.org/10.3390/ijms27114842 - 27 May 2026
Viewed by 212
Abstract
Immune checkpoint inhibitors (ICIs) have transformed the therapeutic landscape of oncology but are increasingly associated with cardiovascular immune-related adverse events (irAEs), including myocarditis, heart failure, arrhythmias, and vascular complications. Among these, ICI-associated myocarditis represents the most severe manifestation, often characterized by high mortality [...] Read more.
Immune checkpoint inhibitors (ICIs) have transformed the therapeutic landscape of oncology but are increasingly associated with cardiovascular immune-related adverse events (irAEs), including myocarditis, heart failure, arrhythmias, and vascular complications. Among these, ICI-associated myocarditis represents the most severe manifestation, often characterized by high mortality and challenging early diagnosis. Detecting subclinical myocardial injury before irreversible cardiomyocyte necrosis occurs remains a major unmet need in contemporary cardio-oncology. This narrative expert review critically examines the biological rationale, preclinical evidence, and emerging clinical data supporting the potential role of heart-type fatty acid-binding protein (H-FABP) as an adjunctive biomarker of early immune-mediated myocardial injury during ICI therapy. H-FABP is a small cytosolic lipid chaperone abundantly expressed in cardiomyocytes and rapidly released into the circulation following subtle membrane destabilization and metabolic stress, frequently preceding detectable troponin elevation in other forms of myocardial injury. Experimental studies support a mechanistic association between H-FABP release, inflammasome activation, cytokine amplification, mitochondrial dysfunction, and immune–metabolic cardiomyocyte stress. Preliminary clinical observations further suggest that H-FABP elevations may occur during ICI treatment even in the absence of overt myocarditis or concomitant increases in high-sensitivity cardiac troponins (hs-cTns). Although H-FABP cannot replace hs-cTn, which remains the cornerstone biomarker for the diagnosis of clinically significant ICI-associated myocarditis, its rapid kinetics and sensitivity to early metabolic membrane injury support its potential role as an investigational adjunctive biomarker for early surveillance and risk stratification. This approach may be particularly relevant in patients receiving high-risk combination ICI regimens or in individuals with pre-existing cardiovascular disease. However, current evidence remains limited, and large prospective multicenter studies integrating H-FABP with hs-cTns, natriuretic peptides, cardiac magnetic resonance imaging, and clinical outcomes are required before routine clinical implementation can be considered. Full article
(This article belongs to the Special Issue Cardioimmunology: Inflammation and Immunity in Cardiovascular Disease—2nd Edition)
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