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Cardioimmunology: Inflammation and Immunity in Cardiovascular Disease
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Cardioimmunology: Inflammation and Immunity in Cardiovascular Disease

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 January 2026 | Viewed by 4163

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 Issue Information

Dear Colleagues,

Peter Libby once told me how he got side-eyed by his peers for calling atherosclerosis an inflammatory disease as an aspiring junior researcher. At that time, the interdisciplinary approach to decipher the intricate interplay between cardiovascular tissue, inflammation and immunity - known as Cardioimmunology today - 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 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 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 (5 papers)

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Research

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17 pages, 4179 KB  
Article
Pattern of Regulatory T Cells, Resident Memory T Cells, and Exhausted T Cells in Human Pericardial Fluid Samples of Cardiovascular Patients
by Barbara Érsek, Júlia Opra, Nóra Fekete, Mandula Ifju, Viktor Molnár, Edina Bugyik, Éva Pállinger, Andrea Székely, Tamás Radovits, Béla Merkely and Edit I. Buzás
Int. J. Mol. Sci. 2025, 26(20), 9852; https://doi.org/10.3390/ijms26209852 - 10 Oct 2025
Viewed by 396
Abstract
This study investigates T cell subsets in pericardial fluid samples obtained from heart transplantation donors, heart transplantation recipients, and coronary artery bypass graft patients. Using flow cytometry, we characterized regulatory T cells (Tregs), tissue-resident memory T cells (Trm), and exhausted T cells based [...] Read more.
This study investigates T cell subsets in pericardial fluid samples obtained from heart transplantation donors, heart transplantation recipients, and coronary artery bypass graft patients. Using flow cytometry, we characterized regulatory T cells (Tregs), tissue-resident memory T cells (Trm), and exhausted T cells based on specific markers. Our results showed significant alterations in the CD4+ and CD8+ T cell subsets, migration (CXCR3, CCR5), and exhaustion markers (PD-1, TIM3) across the groups. Notably, Tregs and Trm cells were enriched in recipients, while markers of T cell exhaustion showed a complex regulation. These findings provide novel insights into the local immune regulation in cardiac disease and transplantation. Full article
(This article belongs to the Special Issue Cardioimmunology: Inflammation and Immunity in Cardiovascular Disease)
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9 pages, 1208 KB  
Article
Mutation of p53 Acetylation Protects Against Angiotensin-II-Induced Cardiac Dysfunction and Fibrosis
by Aubrey C. Cantrell, Quinesha A. Williams, Jian-Xiong Chen and Heng Zeng
Int. J. Mol. Sci. 2025, 26(19), 9668; https://doi.org/10.3390/ijms26199668 - 3 Oct 2025
Viewed by 372
Abstract
Hypertension is a major risk factor for heart failure. Acetylation of p53 is known to regulate its activities. We have previously identified that p53 acetylation is required for cardiac remodeling in a mouse model of pressure overload-induced heart failure. Acetylation mutant p53 (p53aceKO) [...] Read more.
Hypertension is a major risk factor for heart failure. Acetylation of p53 is known to regulate its activities. We have previously identified that p53 acetylation is required for cardiac remodeling in a mouse model of pressure overload-induced heart failure. Acetylation mutant p53 (p53aceKO) mice have been shown to have the ability to regulate SIRT3 KO-induced cardiac fibrosis. In the present study, we hypothesized that p53aceKO mice would exhibit cardiac protection and blunt cardiac fibrosis when subjected to Ang-II-induced hypertension. Control and p53aceKO mice received either a micro-osmotic pump implant administering Ang-II for 28 days or a sham procedure. Blood pressure was measured weekly, and echocardiography was performed every two weeks. Mice were euthanized and hearts were processed for histological analysis. While both control and p53aceKO mice receiving Ang-II exhibit increased systolic and diastolic blood pressures, control mice also demonstrate increases in ejection fraction and fractional shortening compared to the sham, while p53aceKO mice do not. Furthermore, control mice receiving Ang-II exhibit decreased left ventricular diameter and volume at end-systole and end-diastole, as well as thickening of both the anterior and posterior walls, while p53aceKO mice exhibit no significant changes in any of these parameters. Additionally, p53aceKO mice do not exhibit the Ang-II infusion-induced cardiac fibrosis seen in control mice treated with Ang-II. Mutation of p53 acetylation is protective against Ang-II infusion-induced cardiac fibrosis and dysfunction in mice. Acetylated p53 may, therefore, be a novel therapeutic target to address complications in the heart associated with hypertension. Full article
(This article belongs to the Special Issue Cardioimmunology: Inflammation and Immunity in Cardiovascular Disease)
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13 pages, 1204 KB  
Article
Acute Immune Cell Dynamics During Myocardial Infarction and Their Association with Mortality
by Harris Avgousti, Reina Nagasaka, Adovich S. Rivera, Anna Pawlowski, Edward B. Thorp and Matthew J. Feinstein
Int. J. Mol. Sci. 2025, 26(13), 6543; https://doi.org/10.3390/ijms26136543 - 7 Jul 2025
Viewed by 938
Abstract
Acute neutrophil responses following myocardial infarction (MI) play a central role in remodeling, contributing to both repair and potential maladaptive responses. Although prior studies have investigated circulating immune cell indices at a single time point during hospitalization for MI, limited data exist on [...] Read more.
Acute neutrophil responses following myocardial infarction (MI) play a central role in remodeling, contributing to both repair and potential maladaptive responses. Although prior studies have investigated circulating immune cell indices at a single time point during hospitalization for MI, limited data exist on acute intra-individual changes in circulating immune profiles during evolving MI. We analyzed clinical measurements, such as the count and proportion of immune cell components in a serial complete blood count, with differential tests conducted for patients hospitalized with ST-elevation MI (STEMI) in various hospitals in the Northwestern Medicine system from 1 January 2002 to 1 August 2024. Patients with STEMI diagnosis, troponin peaks ≥ 5 ng/mL, and cell count and proportion data prior to the troponin peak and within 24 h after the troponin peak were included. Primary analyses investigated the associations between the troponin peak and peri-STEMI changes in immune cell subsets. Multivariable-adjusted Cox models were used to investigate associations between these peri-STEMI immune cell changes and mortality at 1 year and 3 years. Among the 694 STEMI patients meeting the inclusion criteria, a higher troponin peak was associated with a modest peri-MI increase in neutrophil proportion. Higher adjusted peri-STEMI increases in neutrophil count and proportion were strongly associated with mortality at one and three years [hazard ratio (HR) = 1.31 (95% confidence interval (CI) 1.15–1.49) and HR = 1.27 (95% CI 1.14–1.45) per 1000 cells/μL absolute neutrophil increase, respectively]. Individuals with higher STEMI-related neutrophil increases had higher mortality at one year and three years, independent of the extent of troponin elevation. Full article
(This article belongs to the Special Issue Cardioimmunology: Inflammation and Immunity in Cardiovascular Disease)
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Review

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44 pages, 2818 KB  
Review
Functional Roles of the Complement Immune System in Cardiac Inflammation and Hypertrophy
by Kathryn D. Hok, Haydn E. Rich, Anthony Shadid, Lavanya Gunamalai, Tingting Weng-Mills, Rajarajan A. Thandavarayan, Nirmal K. Banda, Marie-Francoise Doursout, Marcos I. Restrepo and Pooja Shivshankar
Int. J. Mol. Sci. 2025, 26(20), 9931; https://doi.org/10.3390/ijms26209931 - 12 Oct 2025
Viewed by 433
Abstract
Cardiac inflammation and hypertrophy develop as a pathologic response to an array of insults, such as myocardial infarctions, chronic systemic hypertension, and valvular defects. Due to the high prevalence of such conditions, there is an increasing need to prevent and halt cardiac hypertrophy. [...] Read more.
Cardiac inflammation and hypertrophy develop as a pathologic response to an array of insults, such as myocardial infarctions, chronic systemic hypertension, and valvular defects. Due to the high prevalence of such conditions, there is an increasing need to prevent and halt cardiac hypertrophy. Because cardiac damage and subsequent remodeling can lead to arrhythmias, heart failure, and even sudden cardiac death, inhibition of cardiac hypertrophy is key to reducing cardiovascular-related mortality. The immune system is the driving force behind inflammatory reactions. All three pathways of complement system activation—classical, lectin, and alternative—are implicated in developing cardiac damage, inflammation, and hypertrophy due to infectious and non-infectious causes, autoimmune diseases, genetic polymorphisms, and forms of complement dysregulation. Of interest in this review is the role of the complement system, a collection of soluble and membrane-bound proteins that mediate inflammatory processes through interactions with signaling molecules and immune cells. This review comprehensively discusses the roles of these complement pathways in contagious, chronic inflammatory, genetic, and metabolic diseases. An overview of the completed and terminated clinical trials aimed at preventing cardiovascular mortality by targeting various aspects of the complement system and inflammatory reaction is included. Most current treatments for cardiac inflammation and remodeling primarily target the renin–angiotensin–aldosterone system (RAAS), which prevents further remodeling by reducing myocardial workload. However, moving forward, there may be a place for emerging anti-complement therapeutics, which impair the inflammatory response that generates hypertrophy itself. Full article
(This article belongs to the Special Issue Cardioimmunology: Inflammation and Immunity in Cardiovascular Disease)
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29 pages, 2817 KB  
Review
Post-Translational Modifications of Lipoproteins: Emerging Players Linking Inflammation and Cardiovascular Disease in Rheumatoid Arthritis—A Narrative Review
by Chuanhui Xu, Javier Rodríguez-Carrio, Yang Xie, Fanlei Hu, Wei Ming Chong, Han Wei Hou, Rinkoo Dalan and Khai Pang Leong
Int. J. Mol. Sci. 2025, 26(17), 8514; https://doi.org/10.3390/ijms26178514 - 2 Sep 2025
Viewed by 983
Abstract
Patients with rheumatoid arthritis (RA) have an increased risk of cardiovascular disease (CVD) that cannot be fully explained by traditional cardiometabolic risk factors. The observed ‘lipid paradox’, where RA patients with lower total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels exhibit higher CVD [...] Read more.
Patients with rheumatoid arthritis (RA) have an increased risk of cardiovascular disease (CVD) that cannot be fully explained by traditional cardiometabolic risk factors. The observed ‘lipid paradox’, where RA patients with lower total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels exhibit higher CVD risk, may be attributed to post-translational modifications (PTMs). These lipoprotein PTMs likely arise from inflammatory pathways. While PTMs like citrullination and carbamylation are well recognized in RA joint pathology, their occurrence in other protein compartments and their role in CVD have been less well explored. This scoping review summarizes the current literature on PTMs of lipoproteins, including oxidation, nitration, carbamylation, and citrullination, and their impacts on CVD in RA. We also discuss immune responses to these PTMs, their interactions with scavenger receptors, and the effects of disease-modifying antirheumatic drugs. Further research on PTMs may uncover new pathways linking autoimmunity, inflammation, and vascular damage, offering novel diagnostic and therapeutic opportunities for RA-associated CVD. Full article
(This article belongs to the Special Issue Cardioimmunology: Inflammation and Immunity in Cardiovascular Disease)
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