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Cells
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Advances in the Cellular and Molecular Mechanisms of Cardiovascular Diseases
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Advances in the Cellular and Molecular Mechanisms of Cardiovascular Diseases

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

Deadline for manuscript submissions: 31 July 2026 | Viewed by 11061

Special Issue Editors

Prof. Dr. Timothy Martin Palmer

E-Mail Website
Guest Editor
Centre for Biomedicine, Hul York Medical School, University of Hull, Hull HU6 7RX, UK
Interests: vascular endothelium; inflammation; haemostasis; cytokine signalling
Special Issues, Collections and Topics in MDPI journals
Dr. Katie S. Wraith

E-Mail Website
Guest Editor
Centre for Biomedicine, Hull York Medical School, University of Hull, Hull HU6 7RX, UK
Interests: thrombosis; haemostasis; platelets; coagulation

Special Issue Information

Dear Colleagues,

Despite developments in therapeutics that reduce risk factors, such as lipid-lowering drugs, cardiovascular diseases (CVDs) remain the leading cause of death worldwide. Atherosclerotic CVDs encompass a range of conditions leading to serious health complications, such as heart attacks, strokes, and peripheral artery disease. In atherosclerosis, plaque buildup develops within the intima (the innermost layer) of medium- to large-sized arteries, thereby narrowing them and restricting blood flow. Smooth muscle cells also generate a fibrous cap, the properties of which determine sensitivity to plaque rupture and thrombosis. These events are all exacerbated by established risk factors such as high blood pressure, high cholesterol, smoking, and poorly controlled diabetes. Inflammation of the vascular endothelium, immune cell recruitment, smooth muscle dysfunction, and platelet activation status are critical determinants of atherosclerosis. However, despite improvements in revascularisation and pharmacological therapies, new approaches that more effectively target pathophysiological mechanisms responsible for atherosclerosis and atherothrombosis are urgently required.

Prof. Dr. Timothy Martin Palmer
Dr. Katie S. Wraith
Guest Editors

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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

  • thrombosis
  • smooth muscle
  • endothelium
  • atherosclerosis
  • inflammation

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Published Papers (7 papers)

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Research

Jump to: Review

23 pages, 9294 KB  
Article
Strip1 Is a Novel Negative Regulator of Cardiomyocyte Hypertrophy
by Emanuel Heilein, Lucia Sophie Kilian, Samuel Sossalla, Benjamin Meder, Mirko Völkers, Karen S. Frese, Sabine Herch, Norbert Frey and Matthias Eden
Cells 2026, 15(6), 540; https://doi.org/10.3390/cells15060540 - 18 Mar 2026
Viewed by 1409
Abstract
Pathological cardiac hypertrophy is a critical factor leading to cardiomyopathy and ultimately heart failure. While several signaling pathways controlling cardiac hypertrophy have been identified, the molecular mechanisms underlying their precise regulation remain incompletely understood. Strip1, a structural component of STRIPAK complexes, has been [...] Read more.
Pathological cardiac hypertrophy is a critical factor leading to cardiomyopathy and ultimately heart failure. While several signaling pathways controlling cardiac hypertrophy have been identified, the molecular mechanisms underlying their precise regulation remain incompletely understood. Strip1, a structural component of STRIPAK complexes, has been implicated in various cellular functions; however, its role in cardiomyocytes is uncharacterized. Here we identify Strip1 as a potent anti-hypertrophic factor, controlling cell size and the hypertrophic gene program in neonatal rat ventricular cardiomyocytes (NRVCMs). STRIP1 expression was found to be significantly reduced in human dilated and ischemic cardiomyopathies (DCM/ICM), as well as in murine stress model induced by transverse aortic constriction (TAC). In a knockdown model with morpholino-driven STRIP1 reduction in zebrafish in vivo, impaired cardiac function and heart failure–like features were observed. Interestingly, Strip1 localized to the nucleolus in NRVCMs, suggesting a putative nuclear/epigenetic role in cardiomyocytes. Furthermore, our data support association of Strip1 with cardiac STRIPAK complex, modulating kinase activities, including MST1/MST2 and MST4. Mechanistically, Strip1 appears to influence prohypertrophic signaling, including Hippo- and Calcineurin/NFAT-related pathways, which may contribute to pathological cardiac remodeling. Collectively, these findings establish Strip1 as an important modulator of cardiomyocyte hypertrophy and a potential therapeutic target for cardiomyopathy and heart failure. Full article
(This article belongs to the Special Issue Advances in the Cellular and Molecular Mechanisms of Cardiovascular Diseases)
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13 pages, 2853 KB  
Article
Roquin Modulates Cardiac Post-Infarct Remodeling via microRNA Stability Control
by Nadja Itani, Rolf Schreckenberg, Rainer Schulz, Peter Bencsik, Peter Ferdinandy and Klaus-Dieter Schlüter
Cells 2025, 14(22), 1748; https://doi.org/10.3390/cells14221748 - 7 Nov 2025
Viewed by 794
Abstract
Through binding to complementary mRNAs, microRNAs (miRNAs) mediate gene silencing. The stability and half-life of microRNAs are controlled by two isoforms of the RNA-binding protein Roquin. This study aimed at identifying the role of Roquin to miRNA-dependent regulation of the transcriptome in the [...] Read more.
Through binding to complementary mRNAs, microRNAs (miRNAs) mediate gene silencing. The stability and half-life of microRNAs are controlled by two isoforms of the RNA-binding protein Roquin. This study aimed at identifying the role of Roquin to miRNA-dependent regulation of the transcriptome in the post-ischemic heart. Both Roquin isoforms are highly conserved between rats and humans and constitutively expressed in cardiomyocytes. In both cell species, hypoxia induces a down-regulation of Roquin-1 and Roquin-2. An integrative miRNA-and-mRNA analysis (MMIA) identified miR-23b-5p as a potential interaction partner of Roquins. The open data bank TargetScan8.0 suggests that the transcription factor ZBTB20 is a potential target of miR-23b-5p. The level of expression of ZBTB20 correlated with the functional recovery of rat hearts after myocardial infarction. Moreover, the down-regulation of Roquin-2 in AC16 cells by siRNA under normoxic conditions was associated with an up-regulation of miR-23b-5p and a down-regulation of ZBTB20. Furthermore, in the case of hypoxia-dependent down-regulation of Roquin, the subsequent down-regulation of ZBTB20 was reversed with the help of an antagomir against miR-23b-5p. In conclusion, hypoxia-induced down-regulation of the two Roquin isoforms was associated with an increased stability of miR-23b-5p, a Roquin-2-dependent miRNA, which subsequently led to silencing of the transcription factor ZBTB20. Full article
(This article belongs to the Special Issue Advances in the Cellular and Molecular Mechanisms of Cardiovascular Diseases)
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14 pages, 1555 KB  
Article
Ladarixin Potential over the Effects of IL-8 and of Serum from Patients with Abdominal Aortic Aneurysm on Human Aortic Cells
by Lucia Spartano, Maria Lombardi, Vincenzo Ardita, Roberto Chiesa, Andrea Aramini, Marcello Allegretti, Domenico Baccellieri, Lidia De Filippis and Chiara Foglieni
Cells 2025, 14(21), 1713; https://doi.org/10.3390/cells14211713 - 31 Oct 2025
Viewed by 838
Abstract
Early cellular alterations in abdominal aortic aneurysm (AAA) are scarcely investigated. Aortic remodeling inflammation-related suggested the CXCR2/CXCL1/IL-8 axis as a therapeutic target. This study investigates CXCR1/CXCR2 antagonism in primary human aortic endothelial (HAOEC) and smooth muscle cells (HAOSMC) conditioned with IL-8 or serum [...] Read more.
Early cellular alterations in abdominal aortic aneurysm (AAA) are scarcely investigated. Aortic remodeling inflammation-related suggested the CXCR2/CXCL1/IL-8 axis as a therapeutic target. This study investigates CXCR1/CXCR2 antagonism in primary human aortic endothelial (HAOEC) and smooth muscle cells (HAOSMC) conditioned with IL-8 or serum from patients with AAA (sPT). Ladarixin (10 μM Lad or 25 μM) served as an inhibitor. Readouts included RT-qPCR for CXCL1, CXCL8, CXCR2, MMP9, NFKB1, and VEGF-A; zymography for MMP9 activity confocal microscopy for F-actin and mitochondria; NADPH/NADH diaphorase histochemistry for redox activity; and ATP assay. In HAOEC, IL-8 downregulated CXCR2, increased MMP9 activity, and induced cytoskeletal and mitochondria disorganization without altering NADH/NADPH diaphorases but increasing ATP release. At concentration of 10 μM Lad rescued cell organization and gene expression. sPT upregulated CXCL8, CXCR2, and MMP9, decreased NADH/NADPH diaphorases, and altered cytoskeleton and mitochondria organization in HAOEC. At concentration of 10 μM Lad (partially) and 25 μM Lad reverted gene upregulation and mitochondria distribution; both doses increased diaphorase and released ATP. HAOSMC were scantily susceptible to IL-8 and weakly responsive to sPT, slightly upregulating CXCR2 and VEGF-A but increasing proMMP9 gelatinolysis. Ladarixin recovered proMMP9 activity and modulated CXCL1. AAA-like vascular cell alterations involve multiple inflammatory factors and are modulable by inhibition of IL-8 receptors. The results underline careful dose calibration. Full article
(This article belongs to the Special Issue Advances in the Cellular and Molecular Mechanisms of Cardiovascular Diseases)
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18 pages, 2394 KB  
Article
Prostaglandin D2 Synthase: A Novel Player in the Pathological Signaling Mechanism of the Aldosterone–Mineralocorticoid Receptor Pathway in the Heart
by Ankita Garg, Malte Juchem, Sinje Biss, Carla Nunes Borisch, Julia Leonardy, Christian Bär, Shashi Kumar Gupta and Thomas Thum
Cells 2025, 14(19), 1485; https://doi.org/10.3390/cells14191485 - 23 Sep 2025
Viewed by 1679
Abstract
Background: A deregulated aldosterone (Aldo)–mineralocorticoid receptor (MR) pathway is linked to cardiovascular disease (CVD), including hypertension and heart failure. Despite the association of elevated plasma Aldo levels with cardiac stress, inflammation, myocardial fibrosis, and cardiac remodeling, the underlying mechanisms remain elusive. Methods: To [...] Read more.
Background: A deregulated aldosterone (Aldo)–mineralocorticoid receptor (MR) pathway is linked to cardiovascular disease (CVD), including hypertension and heart failure. Despite the association of elevated plasma Aldo levels with cardiac stress, inflammation, myocardial fibrosis, and cardiac remodeling, the underlying mechanisms remain elusive. Methods: To study the impact of Aldo–MR pathway overactivation on cardiac health, a novel mouse model with AAV9-mediated MR overexpression and Aldo administration via subcutaneous osmotic pumps was generated. Echocardiographic analyses, transcriptome sequencing, and loss-of-function experiments of an identified lead candidate gene were performed. Additionally, cardiac tissue samples from human patients with end-stage heart failure were analyzed in the study. Results: Mice with an overactivated Aldo–MR pathway exhibited increased neutrophil gelatinase-associated lipocalin (NGAL) expression, cardiac dysfunction, hypertrophy, and fibrosis. Transcriptomics identified prostaglandin D2 synthase (Ptgds) as a novel downstream effector of the cardiac Aldo–MR pathway. SiRNA-mediated inhibition of Ptgds in primary cardiomyocytes reduced NGAL levels and the hypertrophic impact of Aldo, suggesting a role in mediating Aldo-induced cardiac pathologies. Elevated expression of PTGDS was observed in hiPSC-CMs treated with the pro-hypertrophic cytokine leukemia inhibitory factor (LIF) and in end-stage heart failure patients, ascertaining its importance in cardiac disease settings. Conclusions: PTGDS is a newly identified mediator of Aldo–MR-induced cardiac remodeling and may represent a potential therapeutic target for CVD. Full article
(This article belongs to the Special Issue Advances in the Cellular and Molecular Mechanisms of Cardiovascular Diseases)
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15 pages, 1773 KB  
Article
MicroRNA-21 Protects Hypoxic-Induced Cardiomyocytes Injury by Targeting Smad-7
by Md Sayed Ali Sheikh, A. Alduraywish, Basil Mohammed Alomair, Muhannad Almubarak and Umme Salma
Cells 2025, 14(19), 1483; https://doi.org/10.3390/cells14191483 - 23 Sep 2025
Cited by 2 | Viewed by 1132
Abstract
Globally acute myocardial infarction is the leading independent cause of unexpected death. This study aimed to explore the diagnostic and molecular impact of miR-21, miR-488, and miR-126 in acute myocardial infarction patients (AMI). We enrolled 95 non-ST-elevation myocardial infarction (NSTEMI) patients, 152 ST-elevation [...] Read more.
Globally acute myocardial infarction is the leading independent cause of unexpected death. This study aimed to explore the diagnostic and molecular impact of miR-21, miR-488, and miR-126 in acute myocardial infarction patients (AMI). We enrolled 95 non-ST-elevation myocardial infarction (NSTEMI) patients, 152 ST-elevation myocardial infarction (STEMI) patients, and 95 healthy individuals, additionally using three-month-old mice and their ventricular-derived H9c2 cells. The circulatory plasma miR-21 and miR-488 levels were significantly upregulated, while plasma miR-126 levels were remarkably downregulated in NSTEMI and STEMI subjects. The receiver operating characteristic curve showed that plasma miR-21, miR-488, and miR-126 were able to clearly differentiate NSTEMI and STEMI from healthy subjects. Moreover, H9c2 hypoxic cells treated with inhibitor miR-21 markedly reduced intracellular ROS levels, capase-3 activities levels, and cellular apoptosis rates and significantly enhanced cellular viability through up regulation of Smad-7 mRNA and protein expressions. In geriatric STEMI and NSTEMI subjects, plasma miR-21 levels were evidently higher than in comparatively younger subjects. Upregulated plasma miR-21 and miR-488 levels and downregulated miR-126 levels might be considered potential clinical biomarkers for myocardial infarction patients, while inhibition of miR-21, which significantly reduced hypoxia-exposed H9c2 cellular injury via targeting Smad-7, could be a new therapeutic target for AMI patients. Low levels plasma miR-21 may have a significant impact on delaying the aging process. Full article
(This article belongs to the Special Issue Advances in the Cellular and Molecular Mechanisms of Cardiovascular Diseases)
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Review

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48 pages, 1103 KB  
Review
Inflammatory Mechanisms in Acute Coronary Syndromes: From Pathophysiology to Therapeutic Targets
by Daniel Miron Brie, Cristian Mornoș, Ovidiu Adam, Alexandru Tîrziu, Roxana Popescu and Alina Diduța Brie
Cells 2026, 15(1), 72; https://doi.org/10.3390/cells15010072 - 31 Dec 2025
Cited by 5 | Viewed by 2177
Abstract
Inflammation plays a pivotal role in the pathogenesis of acute coronary syndromes (ACS), contributing to plaque instability, thrombosis, and myocardial injury. This review aims to comprehensively examine the inflammatory mechanisms underlying ACS and evaluate current and emerging anti-inflammatory therapeutic strategies. We conducted a [...] Read more.
Inflammation plays a pivotal role in the pathogenesis of acute coronary syndromes (ACS), contributing to plaque instability, thrombosis, and myocardial injury. This review aims to comprehensively examine the inflammatory mechanisms underlying ACS and evaluate current and emerging anti-inflammatory therapeutic strategies. We conducted a comprehensive literature review examining the role of inflammatory pathways in ACS pathophysiology, including innate and adaptive immune responses, key inflammatory mediators, and cellular mechanisms. We analyzed current evidence for anti-inflammatory therapies and their clinical outcomes in ACS management. Inflammatory processes in ACS involve complex interactions between innate immune cells (neutrophils, macrophages, monocytes) and adaptive immune cells (T lymphocytes, B cells). Key mechanisms include neutrophil extracellular trap (NET) formation, macrophage polarization, T cell subset imbalances (Th1/Th17 predominance with regulatory T cell dysfunction), and complement activation. Inflammatory biomarkers such as C-reactive protein, interleukin-6, and NET-specific markers demonstrate prognostic value. Anti-inflammatory therapies including colchicine, canakinumab (IL-1β inhibition), and methotrexate have shown cardiovascular benefits in clinical trials. Emerging targets include NET inhibition, T cell modulation, and precision inflammatory profiling approaches. Inflammation represents a critical therapeutic target in ACS beyond traditional risk factor modification. While colchicine and IL-1β inhibition have demonstrated clinical efficacy, future strategies should focus on precision medicine approaches targeting specific inflammatory pathways based on individual patient profiles. Integration of anti-inflammatory therapy with lipid management and antithrombotic strategies offers promise for improving ACS outcomes through comprehensive targeting of the multifactorial pathophysiology underlying coronary artery disease. Full article
(This article belongs to the Special Issue Advances in the Cellular and Molecular Mechanisms of Cardiovascular Diseases)
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27 pages, 1759 KB  
Review
Molecular Mechanisms of Atrial Fibrillation Recurrence After Successful Catheter Ablation
by Muhammad Sanusi, Roopeessh Vempati, Dinakaran Umashankar, Suha Tarannum, Yash Varma, Fawaz Mohammed, Maneeth Mylavarapu, Faiza Zakaria, Rajiv Nair, Yeruva Madhu Reddy and Christian Toquica Gahona
Cells 2026, 15(1), 36; https://doi.org/10.3390/cells15010036 - 24 Dec 2025
Cited by 4 | Viewed by 2302
Abstract
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia globally, linked to significant cardiovascular morbidity and mortality. Catheter ablation has emerged as a primary therapeutic approach, yet substantial recurrence rates limit its long-term efficacy. This review critically examines the molecular mechanisms underlying [...] Read more.
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia globally, linked to significant cardiovascular morbidity and mortality. Catheter ablation has emerged as a primary therapeutic approach, yet substantial recurrence rates limit its long-term efficacy. This review critically examines the molecular mechanisms underlying AF recurrence post-ablation, synthesizing recent findings from current literature. Key molecular pathways identified include structural remodeling mediated by fibrosis involving transforming growth factor-beta 1 (TGF-β1) and matrix metalloproteinases (MMPs), ion-channel dysregulation, inflammatory pathways, autonomic nervous system imbalance, and genetic and epigenetic alterations. Despite considerable advances, critical gaps persist due to small, heterogeneous studies and insufficient long-term follow-up. Comprehensive mechanistic research integrating genomics, proteomics, and advanced imaging is urgently needed to better characterize these pathways. Future studies must validate biomarkers such as TGF-β1, MMPs, connexins, and novel markers like GDF-15 and relaxin. Clinical translation of these molecular insights through precision diagnostics and personalized interventions holds great promise to enhance patient selection, optimize ablation strategies, reduce recurrence, and ultimately improve clinical outcomes in AF management. Full article
(This article belongs to the Special Issue Advances in the Cellular and Molecular Mechanisms of Cardiovascular Diseases)
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