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Biomedicines
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Molecular and Cellular Mechanisms of Cardiovascular Diseases: 2nd Edition
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Molecular and Cellular Mechanisms of Cardiovascular Diseases: 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 3923

Special Issue Editor

Dr. Antonella Galeone

E-Mail Website
Guest Editor
Department of Surgery, Dentistry, Pediatrics and Gynecology, Division of Cardiac Surgery, University of Verona, 37134 Verona, Italy
Interests: aortic valve calcification; myocardial ischemia–reperfusion injury; heart failure; heart transplantation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases are a leading cause of death worldwide. This Special Issue, titled “Molecular and Cellular Mechanisms of Cardiovascular Diseases: 2nd Edition”, will focus on the pathophysiology of cardiovascular disorders, including, but not limited to, hypertension, diabetes, coronary artery disease, valvular heart disease, infective endocarditis, aortic dissection and aneurysms, heart failure, congenital and acquired cardiomyopathies, and cardiac tumors. This Special Issue will focus on known and new signaling pathways involved in the large spectrum of cardiovascular diseases, affecting calcium homeostasis, mitochondria and energy metabolism, oxidative stress, inflammation, cardiac cell survival and apoptosis, autophagy, and the extracellular matrix. In addition, the alteration of hormonal and neurohormonal signaling, including adrenergic systems, renin–angiotensin–aldosterone systems, and sex hormones, and the molecular and cellular mechanisms leading to gender differences in cardiovascular disease will be included in this Special Issue. This Special Issue aims to provide a better understanding of the molecular and cellular mechanisms leading to cardiovascular disease that have not yet been fully elucidated. Furthermore, our aim is to gain a general overview of known and new therapeutic approaches and drug targets in the field. Comprehensive reviews and original research (basic, translational, or clinical research) providing new insights into the molecular and cellular mechanisms leading to cardiovascular disease, including novel therapeutic approaches, are welcome.

Dr. Antonella Galeone
Guest Editor

Manuscript Submission Information

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Keywords

  • hypertension
  • diabetes
  • coronary heart disease
  • valvular heart disease
  • infective endocarditis
  • aortic dissection
  • aortic aneurysm
  • heart failure
  • cardiomyopathy

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Related Special Issue

Published Papers (4 papers)

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Research

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17 pages, 1101 KB  
Article
Age-Dependent Inflammatory, Lipid, and Echocardiographic Phenotypes in Acute Myocardial Infarction: Associations with In-Hospital Adverse Clinical Events
by Bogdan-Sorin Tudurachi, Larisa Anghel, Andreea Tudurachi, Radu Andy Sascău, Cristian Stătescu, Mircea Ovanez Balasanian, Nicoleta Dubei and Delia Șalaru
Biomedicines 2026, 14(5), 1066; https://doi.org/10.3390/biomedicines14051066 - 8 May 2026
Viewed by 650
Abstract
Background: Acute myocardial infarction (AMI) in younger adults represents a distinct clinical entity with biological features that may differ from those observed in later-onset disease. We aimed to characterize age-dependent clinical, inflammatory, lipid, and echocardiographic phenotypes and to explore their association with in-hospital [...] Read more.
Background: Acute myocardial infarction (AMI) in younger adults represents a distinct clinical entity with biological features that may differ from those observed in later-onset disease. We aimed to characterize age-dependent clinical, inflammatory, lipid, and echocardiographic phenotypes and to explore their association with in-hospital adverse clinical events. Methods: In this prospective, single-center, age-stratified observational study conducted between 20 January 2024 and 20 January 2025, 90 patients with AMI undergoing successful percutaneous coronary intervention (PCI) were selected from 1051 AMI admissions: 30 aged 25–44 years and 60 aged ≥45 years. Admission biomarkers (including C-reactive protein, leukocyte-derived indices, and lipid parameters) and echocardiographic variables (left ventricular ejection fraction and global longitudinal strain) were assessed, and exploratory receiver operating characteristic analyses were performed for in-hospital adverse clinical events. Results: Younger patients demonstrated a predominantly atherogenic profile, with higher smoking prevalence (63.3% vs. 13.3%; p < 0.001) and markedly higher lipoprotein(a) concentrations (76.18 ± 10.10 vs. 17.61 ± 11.42 mg/dL; p < 0.001). Older patients exhibited higher inflammatory indices (NLR and SII), higher hs-cTnI and NT-proBNP concentrations, and worse ventricular function. STEMI predominated in both age groups (83.3% in each), and infarct localization did not differ significantly between younger and older patients. The rate of in-hospital adverse clinical events was numerically higher in older patients (18.3% vs. 10.0%), but this difference was not statistically significant. In exploratory ROC analyses, CRP (AUC = 0.874) and LVEF (AUC = 0.868) showed the highest discriminatory performance. Conclusions: AMI appears to manifest through age-related baseline phenotypes: a more atherogenic/thrombotic profile in younger patients and a more inflammatory/ventricular dysfunction profile in older patients. CRP and LVEF emerged as the strongest exploratory discriminators of in-hospital adverse clinical events, but these findings require validation in larger cohorts. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cardiovascular Diseases: 2nd Edition)
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16 pages, 1055 KB  
Article
Relationship Between Mitral Annular Calcification and Inflammatory Indices in Patients with Cardiometabolic Risk Factors
by Paula Cristina Morariu, Alexandru Florinel Oancea, Maria Mihaela Godun, Diana Elena Floria, Oana Sîrbu, Anca Ouatu, Daniela Maria Tanase, Ionela Daniela Morariu, Cristina Gena Dascălu and Mariana Floria
Biomedicines 2026, 14(2), 398; https://doi.org/10.3390/biomedicines14020398 - 9 Feb 2026
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Abstract
Background: Mitral annular calcification (MAC) is associated with systemic atherosclerosis and cardiometabolic risk factors. Although hematologic inflammatory indices have been reported to be correlated with MAC, whether these associations persist after accounting for the cardiometabolic context in which MAC occurs remains unclear. Methods: [...] Read more.
Background: Mitral annular calcification (MAC) is associated with systemic atherosclerosis and cardiometabolic risk factors. Although hematologic inflammatory indices have been reported to be correlated with MAC, whether these associations persist after accounting for the cardiometabolic context in which MAC occurs remains unclear. Methods: In a prospective, cross-sectional study of consecutive adults, patients with mild MAC were compared to those without MAC. Individuals with major inflammatory conditions, advanced chronic kidney disease, cirrhosis, malignancy, autoimmune/acute inflammatory disorders, significant valvular disease, prosthetic valves/pacing devices, psychiatric disorders, or moderate-severe MAC were excluded. C-reactive protein (CRP) and hematological inflammatory indices, including neutrophil-to-lymphocyte ratio (NLR), Systemic Inflammatory Response Index (SIRI), and lymphocyte-to-leukocyte ratio (LLR), were analyzed in relation to MAC status. Results: Among 205 patients, 134 had mild MAC and 71 had no MAC. Patients with MAC were older and displayed higher cardiometabolic burden, including more frequent dysglycemia, higher blood pressure, and greater adiposity. In unadjusted comparisons, inflammatory markers differed according to MAC status: CRP (0.31 mg/dL vs. 0.18 mg/dL, p = 0.002), NLR (2.52 vs. 1.99, p = 0.032), SIRI (1.27 vs. 1.04, p = 0.039), and LLR (0.26 vs. 0.29, p = 0.032). In multivariable logistic regression models, none of the inflammatory markers remained independently associated with MAC. In contrast, age (ORs 1.056–1.063 per year increase, p ≤ 0.001), prediabetes (ORs 2.43–3.63, p ≤ 0.001), and type 2 diabetes (OR 5.91 and 6.19, p ≤ 0.001) demonstrated consistent independent associations with MAC across all models. Conclusions: In this cardiometabolic population with mild MAC, inflammatory indices showed unadjusted differences but no independent associations with MAC after comprehensive cardiometabolic adjustment. These findings are most compatible with inflammatory markers primarily reflecting the cardiometabolic milieu in which MAC occurs rather than representing MAC-specific processes. Age and glucose metabolism abnormalities emerged as the dominant independent factors associated with mild MAC, reinforcing the central role of metabolic dysfunction in MAC pathogenesis. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cardiovascular Diseases: 2nd Edition)
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Review

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23 pages, 554 KB  
Review
The Role of GH-IGF-1 Axis and S-Klotho in Atherosclerosis Natural History, Plaque Phenotype and Vulnerability: A Narrative Review
by Angela Buonpane, Salvatore Raia, Giancarlo Trimarchi, Donato Antonio Paglianiti, Fabio Casamassima, Giorgio Maria Orazi, Carlo Trani, Filippo Crea, Giovanna Liuzzo, Francesco Burzotta and Antonio Bianchi
Biomedicines 2026, 14(4), 775; https://doi.org/10.3390/biomedicines14040775 - 29 Mar 2026
Viewed by 714
Abstract
Atherosclerosis is a complex, multifactorial disease that progresses through distinct stages: initiation, progression, and complication, ultimately leading to acute coronary syndromes (ACS). Endothelial cells (ECs), vascular smooth muscle cells (VSMCs), and macrophages are central players in this process, influencing plaque stability and vulnerability. [...] Read more.
Atherosclerosis is a complex, multifactorial disease that progresses through distinct stages: initiation, progression, and complication, ultimately leading to acute coronary syndromes (ACS). Endothelial cells (ECs), vascular smooth muscle cells (VSMCs), and macrophages are central players in this process, influencing plaque stability and vulnerability. Insulin-Like Growth Factor 1 (IGF-1), soluble-Klotho (S-Klotho), and the Growth Hormone Receptor exon 3 deletion polymorphism (GHRd3) have emerged as key modulators of vascular health, impacting these cellular components through various mechanisms. IGF-1 supports endothelial function, enhances VSMC survival and migration, and mitigates inflammation by inhibiting macrophage recruitment and activation, ultimately reducing the risk of plaque destabilization. S-Klotho, an anti-aging protein with potent anti-inflammatory and antioxidant properties, has been linked to vascular protection, with its deficiency associated with endothelial dysfunction, vascular calcification, and impaired VSMC survival. Evidence suggests that IGF-1 may enhance Klotho shedding, indicating a potential synergistic role in maintaining vascular integrity. This narrative review aims to outline the fundamental stages of atherosclerosis progression, consolidate current evidence on the roles of IGF-1 and S-Klotho in modulating key cellular components of atherosclerosis, and shed light on their potential involvement in plaque healing—an area that remains largely unexplored. By integrating established molecular mechanisms, we explore how these factors may contribute to endothelial integrity, VSMC survival, and macrophage activation and polarization, potentially shaping a more stable plaque phenotype and influencing future therapeutic strategies in cardiovascular disease. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cardiovascular Diseases: 2nd Edition)
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32 pages, 3665 KB  
Review
Structural and Functional Regulation of RyR2 in Cardiac Calcium Handling and Arrhythmogenesis
by Kaiyang Gao, Wenzhuo Wang, Yanan Ling, Baihe Li, Chenlei Xing, Nike Li, Xiaolan Yin, Lan Tao, Xiaoqing Li, Junling Qiu, Xuanqi Wang and Jinhong Wei
Biomedicines 2026, 14(3), 662; https://doi.org/10.3390/biomedicines14030662 - 14 Mar 2026
Cited by 1 | Viewed by 1284
Abstract
Cardiac Ca2+ handling is critical for excitation–contraction coupling (ECC), with the ryanodine receptor type 2 (RyR2) serving as the key sarcoplasmic reticulum (SR) Ca2+ release channel in cardiomyocytes. The dysfunction of RyR2 is linked to fatal cardiac arrhythmias, including heart failure [...] Read more.
Cardiac Ca2+ handling is critical for excitation–contraction coupling (ECC), with the ryanodine receptor type 2 (RyR2) serving as the key sarcoplasmic reticulum (SR) Ca2+ release channel in cardiomyocytes. The dysfunction of RyR2 is linked to fatal cardiac arrhythmias, including heart failure (HF) and catecholaminergic polymorphic ventricular tachycardia (CPVT). This review aims to elucidate the structural basis of RyR2, its core role in cardiac ECC and Ca2+ homeostasis, and the regulatory mechanisms of key modulators on its activity. By integrating recent high-resolution cryo-EM structural analyses with molecular and cellular studies on RyR2 regulation, as well as clinical evidence of RyR2 mutations in arrhythmogenic heart diseases, we provide a comprehensive overview of the field. Cryo-EM has unraveled RyR2’s gating mechanisms, ligand-binding sites, and structural features. Functionally, RyR2 mediates calcium-induced calcium release (CICR) and maintains Ca2+ homeostasis through coordination with SERCA2a and NCX. Key modulators (CaM, FKBP12.6, and PKA/CaMKII) and disease-linked mutations regulate RyR2 activity through distinct pathways, with defective RyR2 leading to store-overload-induced Ca2+ release (SOICR) and arrhythmias. Furthermore, reactive oxygen species (ROS) can induce RyR2 oxidation, establishing a pathological Ca2+ leak-ROS cycle in heart disease. In conclusion, RyR2 is a pivotal sensor of myocardial function, with its structural and regulatory mechanisms now well-characterized by recent studies. However, the effects of numerous RyR2 mutations remain unclear, and deeper mechanistic insights will lay a key foundation for developing novel therapies against RyR2-related cardiac diseases. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cardiovascular Diseases: 2nd Edition)
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