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Cells
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New Research on Immunity and Inflammation in Cardiovascular Disease
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New Research on Immunity and Inflammation in Cardiovascular Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 7582

Special Issue Editor

Prof. Dr. Pavel Poredoš

E-Mail Website
Guest Editor
Department for Vascular Diseases, University of Ljubljana, Ljubljana, Slovenia
Interests: cardiovascular disease and inflammation; preclinical atherosclerosis; endothelial dysfunction; intima-media thickness
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The basic pathogenetic mechanisms of cardiovascular (CV) disease remain poorly understood. Recent evidence shows that immuno-inflammatory activity plays a pivotal role in many CV diseases. Atherosclerosis, as the most frequent cardiovascular disease, is primarily a chronic inflammatory disease of the arterial wall. Inflammation induces endothelial dysfunction, which results in an increased permeability of the vessel wall to lipoproteins and their sub-endothelial accumulation. It also induces leukocyte recruitment and platelet activation, which is followed by atherosclerotic plaque formation and CV events. Inflammation is a common mechanism that links traditional risk factors to the development of atherosclerosis. Inflammation is a critical feature of vulnerable plaques, which influences their stability and related thromboembolic complications. In addition, inflammatory pathways may be leading mechanisms in other CV diseases, including heart failure, cardiomyopathies, and rhythm disorders. Inflammation is also involved in the pathogenesis of venous thromboembolic diseases and chronic venous insufficiency. Inflammation of the vessel wall is specifically caused by a large family of chemotactic cytokines, known as chemokines. The intensity of inflammatory processes can be determined by establishing the levels of circulating inflammatory markers, which also serve as potential biomarkers of disease severity and prognosis.

In the proposed Special Issue, “New Research on Immunity and Inflammation in Cardiovascular Disease”, we would like to elucidate the role of inflammation in the pathogenesis of different atherosclerotic CV diseases and its involvement in venous diseases. In addition, the utility of circulating inflammatory markers in determining disease severity and prognosis will be discussed. Finally, the role of the anti-inflammatory treatment of CV disease will be described.

Prof. Dr. Pavel Poredoš
Guest Editor

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • inflammation
  • atherosclerosis
  • coronary artery disease
  • peripheral arterial disease
  • cerebrovascular disease
  • venous thromboembolic disease
  • circulating biomarkers
  • anti-innflammatory treatment of cardiovascular disease

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Published Papers (7 papers)

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Research

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24 pages, 4260 KB  
Article
Distinct Inflammatory Responses of hiPSC-Derived Endothelial Cells and Cardiomyocytes to Cytokines Involved in Immune Checkpoint Inhibitor-Associated Myocarditis
by Samantha Conte, Isaure Firoaguer, Simon Lledo, Thi Thom Tran, Claire El Yazidi, Stéphanie Simoncini, Zohra Rebaoui, Claire Guiol, Christophe Chevillard, Régis Guieu, Denis Puthier, Franck Thuny, Jennifer Cautela and Nathalie Lalevée
Cells 2025, 14(17), 1397; https://doi.org/10.3390/cells14171397 - 7 Sep 2025
Viewed by 844
Abstract
Inflammatory cytokines, particularly interferon-γ (IFN-γ), are markedly elevated in the peripheral blood of patients with immune checkpoint inhibitor-induced myocarditis (ICI-M). Endomyocardial biopsies from these patients also show GBP-associated inflammasome overexpression. While both factors are implicated in ICI-M pathophysiology, their interplay and cellular targets [...] Read more.
Inflammatory cytokines, particularly interferon-γ (IFN-γ), are markedly elevated in the peripheral blood of patients with immune checkpoint inhibitor-induced myocarditis (ICI-M). Endomyocardial biopsies from these patients also show GBP-associated inflammasome overexpression. While both factors are implicated in ICI-M pathophysiology, their interplay and cellular targets remain poorly characterized. Our aim was to elucidate how ICI-M-associated cytokines affect the viability and inflammatory responses of endothelial cells (ECs) and cardiomyocytes (CMs) using human induced pluripotent stem cell (hiPSC)-derived models. ECs and CMs were differentiated from the same hiPSC line derived from a healthy donor. Cells were exposed either to IFN-γ alone or to an inflammatory cytokine cocktail (CCL5, GZMB, IL-1β, IL-2, IL-6, IFN-γ, TNF-α). We assessed large-scale transcriptomic changes via microarray and evaluated inflammatory, apoptotic, and cell death pathways at cellular and molecular levels. hiPSC-ECs were highly sensitive to cytokine exposure, displaying significant mortality and marked transcriptomic changes in immunity- and inflammation-related pathways. In contrast, hiPSC-CM showed limited transcriptional changes and reduced susceptibility to cytokine-induced death. In both cell types, cytokine treatment upregulated key components of the inflammasome pathway, including regulators (GBP5, GBP6, P2X7, NLRC5), a core component (AIM2), and the effector GSDMD. Increased GBP5 expression and CASP-1 cleavage mirrored the findings found elsewhere in endomyocardial biopsies from ICI-M patients. This hiPSC-based model reveals a distinct cellular sensitivity to ICI-M-related inflammation, with endothelial cells showing heightened vulnerability. These results reposition endothelial dysfunction, rather than cardiomyocyte injury alone, as a central mechanism in ICI-induced myocarditis. Modulating endothelial inflammasome activation, particularly via AIM2 inhibition, could offer a novel strategy to mitigate cardiac toxicity while preserving antitumor efficacy. Full article
(This article belongs to the Special Issue New Research on Immunity and Inflammation in Cardiovascular Disease)
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28 pages, 27512 KB  
Article
Wire Injury-Induced Moderate Aortic Valve Stenosis in Mice Is Accompanied by a Chronic Systemic Inflammatory Reaction
by Katrin Becker
Cells 2025, 14(12), 883; https://doi.org/10.3390/cells14120883 - 11 Jun 2025
Cited by 1 | Viewed by 770
Abstract
Background/Objectives: While the presence of inflammatory processes in stenotic aortic valves is acknowledged, no systematic characterization of the systemic immune reaction upon aortic valve stenosis (AS) has been performed yet. The hypothesis of this study was that AS induces a systemic inflammatory reaction [...] Read more.
Background/Objectives: While the presence of inflammatory processes in stenotic aortic valves is acknowledged, no systematic characterization of the systemic immune reaction upon aortic valve stenosis (AS) has been performed yet. The hypothesis of this study was that AS induces a systemic inflammatory reaction linked with local processes in the heart. Methods: Murine wire injury (WI) to induce AS, or sham surgery, were performed prior to the 4-week assessment of AS severity, left ventricular (LV) function and hypertrophy with echocardiography (echo). Organ weights, levels of leukocytes, cytokines and costimulatory molecules in blood, heart, and peripheral immune organs (spleen, liver, lymph nodes), and immune cell uptake of Cy5-labelled perfluorocarbon nanoemulsions were measured. Results: Trends towards correlation were found between organ weights, myocardial immune cells and echo. Cytokine mRNA levels trended mainly towards an increase in heart and regional lymph nodes and a reduction in spleen and liver, and correlation with echo was more homogeneous after WI. Unchanged cytokine protein levels in myocardium and plasma trended to correlate with echo. A homogeneous pattern was found for echo and costimulatory molecule correlation, while PFC uptake by lymphatic cells was reduced upon AS. Conclusions: The results suggest a link between number and activation state of leukocytes in peripheral organs and cardiac processes in AS. Considering the pathological value of inflammation, it is crucial that future studies investigate if a modulation of the systemic inflammatory reaction relieves severity of AS and opposes development of heart failure. Full article
(This article belongs to the Special Issue New Research on Immunity and Inflammation in Cardiovascular Disease)
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Review

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21 pages, 1901 KB  
Review
Targeting the NO–sGC–cGMP Pathway: Mechanisms of Action of Vericiguat in Chronic Heart Failure
by Tine Bajec and Gregor Poglajen
Cells 2025, 14(17), 1400; https://doi.org/10.3390/cells14171400 - 8 Sep 2025
Viewed by 1200
Abstract
The recent advancements in the medical management of patients with chronic heart failure with reduced ejection fraction (HFrEF) is the soluble guanylate cyclase (sGC) stimulator, vericiguat. Clinical trials have demonstrated that vericiguat effectively lowers plasma levels of NT-proBNP and reduces the risk of [...] Read more.
The recent advancements in the medical management of patients with chronic heart failure with reduced ejection fraction (HFrEF) is the soluble guanylate cyclase (sGC) stimulator, vericiguat. Clinical trials have demonstrated that vericiguat effectively lowers plasma levels of NT-proBNP and reduces the risk of cardiovascular death or hospitalization in HFrEF patients, making it a class IIb recommendation for patients with worsening heart failure despite receiving guideline-directed medical therapy. However, the precise pathophysiological mechanisms underlying these clinical benefits remain unexplored. This review aims to present the signalling pathways associated with maladaptive remodeling and heart failure progression that can be modulated by sGC stimulators, focusing on the antihypertrophic, antifibrotic, and anti-inflammatory effects of NO–sGC–cGMP signalling observed in preclinical studies. A better understanding of the mechanisms of action of sGC stimulators could optimize heart failure treatment strategies and enable tailoring of therapies to individual patient profiles. Full article
(This article belongs to the Special Issue New Research on Immunity and Inflammation in Cardiovascular Disease)
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23 pages, 2478 KB  
Review
Senescent Polarization of Macrophages and Inflammatory Biomarkers in Cardiovascular Disease
by Alojz Ihan
Cells 2025, 14(17), 1374; https://doi.org/10.3390/cells14171374 - 3 Sep 2025
Viewed by 984
Abstract
Cardiovascular diseases (CVDs) are a group of disorders in which inflammatory processes play a crucial role. Age-related chronic systemic inflammation is characterized by elevated levels of inflammatory mediators in the bloodstream. It can occur even in the absence of overt infection, contributing to [...] Read more.
Cardiovascular diseases (CVDs) are a group of disorders in which inflammatory processes play a crucial role. Age-related chronic systemic inflammation is characterized by elevated levels of inflammatory mediators in the bloodstream. It can occur even in the absence of overt infection, contributing to endothelial dysfunction, vascular stiffness, and atherosclerosis. The regulation of vascular tissue homeostasis and inflammation is primarily mediated by tissue-resident macrophages (TRMs) and monocyte-derived macrophages. The proportion of monocyte-derived macrophages increases with age, contributing to vascular damage and accelerating CVD progression. In aging tissue, monocyte-derived macrophages exposed to various microenvironmental stimuli are predominantly polarized into the pro-inflammatory M1 phenotype. This polarization, in turn, triggers the release of pro-inflammatory cytokines (IL-1β, IL-6, and IL-18) and promotes the generation of oxidative stress molecules. In this review, we examine the role of macrophages in cardiovascular aging, their secretory phenotypes, and the impact of chronic low-grade inflammation on vascular integrity. We also propose reliable biomarkers of chronic cardiovascular inflammation that may aid in risk prediction, patient stratification, and the development of senotherapeutic interventions for cardiovascular disease. Full article
(This article belongs to the Special Issue New Research on Immunity and Inflammation in Cardiovascular Disease)
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13 pages, 266 KB  
Review
Inflammation and Perioperative Cardiovascular Events
by Peter Poredos and Radko Komadina
Cells 2025, 14(17), 1362; https://doi.org/10.3390/cells14171362 - 1 Sep 2025
Viewed by 731
Abstract
Surgery and anesthesia induce a stress response that provokes increased sympathetic stimulation, secretion of cortisol, hypercoagulability, and systemic inflammatory response. All these homeostatic deteriorations, especially systemic inflammation, represent a risk for organ damage. Perioperative cardiac complications have an increasing impact on morbidity and [...] Read more.
Surgery and anesthesia induce a stress response that provokes increased sympathetic stimulation, secretion of cortisol, hypercoagulability, and systemic inflammatory response. All these homeostatic deteriorations, especially systemic inflammation, represent a risk for organ damage. Perioperative cardiac complications have an increasing impact on morbidity and mortality, not only in cardiovascular but also in non-cardiac surgery. Surgical procedures represent a potential trigger for systemic inflammation that causes secretion of proinflammatory cytokines, activation of neutrophils, and tissue damage. Also, increased levels of preoperative inflammatory markers predict perioperative cardiovascular events. Systemic inflammatory biomarkers increase during the first days after surgical procedures and decline within a few weeks. Besides contemporary traditional biomarkers (CRP, BNP), newer biomarkers, such as galectin-3, TNF-α, and various MiRNAs, can predict inflammatory response and related cardiac injury. Determination of inflammatory markers in the perioperative period could help identify patients at risk for cardiovascular events. The reduction in perioperative inflammatory response may improve surgical outcomes. Prevention and treatment of systemic inflammation can be achieved by optimization of surgical procedures, anesthetic regimen, and pharmacological agents, especially interleukin inhibitors. Determination of inflammatory biomarkers, along with prevention and treatment of inflammation, can improve perioperative cardiac risk reduction strategies. Full article
(This article belongs to the Special Issue New Research on Immunity and Inflammation in Cardiovascular Disease)
12 pages, 237 KB  
Review
Inflammation—A Link Between Arterial Atherosclerotic and Venous Thromboembolic Diseases
by Pavel Poredos and Peter Poredos
Cells 2025, 14(17), 1319; https://doi.org/10.3390/cells14171319 - 27 Aug 2025
Viewed by 1063
Abstract
An increasing body of evidence suggests the likelihood of a link between arterial atherosclerotic disease (AAD) and venous thromboembolic disease (VTED). Inflammation is accepted as a basic pathogenetic mechanism of both diseases. The involvement of inflammation in the pathogenesis of AAD and VTED [...] Read more.
An increasing body of evidence suggests the likelihood of a link between arterial atherosclerotic disease (AAD) and venous thromboembolic disease (VTED). Inflammation is accepted as a basic pathogenetic mechanism of both diseases. The involvement of inflammation in the pathogenesis of AAD and VTED is supported by increased levels of circulating inflammatory markers, particularly interleukins, which are involved in the development and progression of atherosclerosis as well as in thrombus formation in arterial and venous beds. A consideration supporting a close link between these diseases is also based on the evidence of common risk factors which promote the development of both diseases through stimulation of systemic inflammation. Further, the relationship between arterial and VTED is supported by findings of the simultaneous appearance of clinical or preclinical AAD and VTED. The aim of this narrative review is to report evidence of the inflammatory basis of arterial and venous diseases, which is important for common therapeutic procedures. Besides classical drugs used in the prevention of arterial and venous diseases with their pleotropic anti-inflammatory activity, new anti-inflammatory drugs provide the possibility for treatment of both AAD and VTED and could represent a unified therapeutic approach to both diseases. Full article
(This article belongs to the Special Issue New Research on Immunity and Inflammation in Cardiovascular Disease)
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Other

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18 pages, 836 KB  
Systematic Review
The Interplay Between Autoimmune Disorders Affecting the Coagulation and Platelet Systems and Their Implications for Cardiovascular Diseases: A Systematic Review
by Kiana Mohammadian, Melika Asayesh, Fatemeh Fakhar, Shayan Keramat and Agata Stanek
Cells 2025, 14(13), 1023; https://doi.org/10.3390/cells14131023 - 4 Jul 2025
Viewed by 1108
Abstract
Autoimmune diseases (AIDs) are chronic, heterogeneous conditions developing from an aberrant immune response, impacting particular organs or multiple systems. This systematic review attempted to investigate and evaluate the correlation between autoimmune diseases and cardiovascular disease (CVD), emphasizing immunological and pathophysiological mechanisms. A comprehensive [...] Read more.
Autoimmune diseases (AIDs) are chronic, heterogeneous conditions developing from an aberrant immune response, impacting particular organs or multiple systems. This systematic review attempted to investigate and evaluate the correlation between autoimmune diseases and cardiovascular disease (CVD), emphasizing immunological and pathophysiological mechanisms. A comprehensive search for relevant research was conducted on the PubMed, SCOPUS, and ScienceDirect databases, resulting in the identification of 28 studies that met the inclusion criteria. Of the cohort studies, 26 (92.8%) demonstrated a significant association between autoimmune diseases and increased cardiovascular risk. The major mechanisms include chronic inflammation, endothelial dysfunction, oxidative stress, and immune cell dysregulation. Essential biological components, including T cells, B cells, and neutrophils, were identified as contributors to atherosclerotic processes through cytokine secretion, expression of adhesion molecules, and thrombogenic activity. In contrast, two studies (7.1%) found no statistically significant association. In conclusion, autoimmune diseases significantly increase cardiovascular risk through complicated immunological mechanisms. Comprehending these pathways could influence future therapeutic approaches to reduce cardiovascular complications in affected patients. Full article
(This article belongs to the Special Issue New Research on Immunity and Inflammation in Cardiovascular Disease)
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