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Biology
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Advances in Cardiac and Vascular Biology: From Mechanisms to Pathophysiology
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Advances in Cardiac and Vascular Biology: From Mechanisms to Pathophysiology

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Physiology".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 4197

Special Issue Editors

Dr. Hanqiang Deng

E-Mail Website
Guest Editor
Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, School of Medicine, Yale University, New Haven, CT 06511, USA
Interests: cardiovascular diseases; vascular remodeling; inflammation; fluid shear stress; metabolism
Dr. Haodi Wu

E-Mail Website
Guest Editor
Heart, Lung, Blood, and Vascular Medicine Institute, Department of Medicine, Division of Cardiology, University of Pittsburgh, Pittsburgh, PA 15260, USA
Interests: induced pluripotent stem cell model; inherited cardiomyopathies; calcium handling; genome editing; cardiac arrhythmias; cardiac aging; heart failure

Special Issue Information

Dear Colleagues,

The heart and blood vessels form a highly integrated system, governed by intricate molecular and cellular interactions that are essential for maintaining cardiovascular functions and homeostasis. Disruptions in these processes contribute to a broad spectrum of cardiovascular diseases, the leading cause of morbidity and mortality worldwide.

This Special Issue aims to enhance our understanding of cardiovascular pathophysiology at both the molecular and cellular levels, encouraging new perspectives in basic cardiovascular research. It will focus on fundamental biological mechanisms that drive cardiac and vascular development, homeostasis, and disease progression. The emphasis will be on novel insights into signaling pathways, cellular crosstalk, genomic and epigenomic regulation, and metabolic adaptations in cardiac and vascular physiology and pathology.

Key topics of interest include, but are not limited to, the following:

  • Endothelial and smooth muscle cell dynamics;
  • Cardiomyocyte biology;
  • Stem cell biology and tissue regeneration;
  • Extracellular matrix remodeling;
  • Mechanotransduction;
  • Metabolic reprogramming;
  • Genomic and epigenomic regulation;
  • Autophage and protein homeostasis;
  • The role of non-coding RNAs in cardiovascular regulation.

We invite the submission of original studies and comprehensive reviews that illuminate these critical biological processes.

Dr. Hanqiang Deng
Dr. Haodi Wu
Guest Editors

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. Biology is an international peer-reviewed open access semimonthly journal published by MDPI.

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

  • cardiovascular biology
  • molecular mechanisms
  • cellular signaling
  • epigenomic regulation
  • vascular remodeling
  • metabolic reprogramming
  • cardiac pathophysiology

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (4 papers)

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Research

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18 pages, 4940 KB  
Article
FGF23 Controls Myocardial Fibrosis Progression via Promoting Cardiac Fibroblast Proliferation and Activation in Mice
by Leyi Shen, Mingqi Hu, Mei Xue and Santie Li
Biology 2026, 15(7), 539; https://doi.org/10.3390/biology15070539 - 27 Mar 2026
Viewed by 596
Abstract
Heart failure (HF) is the leading cause of morbidity and mortality worldwide, while myocardial fibrosis acts as a pivotal hallmark, which exacerbates ventricular dysfunction and remodeling in HF. In this study, we found FGF23, a critical endocrine regulator, which regulates phosphate and vitamin [...] Read more.
Heart failure (HF) is the leading cause of morbidity and mortality worldwide, while myocardial fibrosis acts as a pivotal hallmark, which exacerbates ventricular dysfunction and remodeling in HF. In this study, we found FGF23, a critical endocrine regulator, which regulates phosphate and vitamin D metabolism, was significantly upregulated in fibrotic mouse hearts after transverse aortic constriction (TAC). By using the FGF23 monoclonal antibody, we found that inhibition of FGF23 alleviated TAC-induced cardiac fibrosis, while injection of recombinant FGF23 (rFGF23) protein exacerbated tissue fibrosis in mouse hearts after TAC. RNA sequencing indicated that FGF23 may promote cardiac fibroblast proliferation and activation in stressed mouse hearts. In human primary cardiac fibroblasts, rFGF23 treatment further upregulated the expression of Ki67, Cyclin D1, Cyclin E1, PCNA, α-SMA, and collagen 1A1 after TGF-β stimulation. Further results indicated that FGF23 promoted cardiac fibroblast proliferation and activation through FGFR4 and activated the downstream MAPK/ERK signaling. This study suggests a role of FGF23 in the regulation of myocardial fibrosis, which shows the potential of targeting FGF23 in the treatment of HF and cardiac fibrosis. Full article
(This article belongs to the Special Issue Advances in Cardiac and Vascular Biology: From Mechanisms to Pathophysiology)
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18 pages, 2436 KB  
Article
Induction of Autoimmune Myocarditis in Diversity Outbred Mice
by Meghna Sur, Kiruthiga Mone, Shraddha Singh, Mahima T. Rasquinha, Jean-Jack M. Riethoven, Indranil Mukhopadhyay, Raymond A. Sobel and Jay Reddy
Biology 2026, 15(3), 288; https://doi.org/10.3390/biology15030288 - 6 Feb 2026
Viewed by 1110
Abstract
Background. Inbred mouse models of autoimmune myocarditis are routinely used to investigate the immune mechanisms underlying dilated cardiomyopathy. However, their translational relevance is limited because observations made in a single inbred strain may not reflect those of outbred human populations. This limitation can [...] Read more.
Background. Inbred mouse models of autoimmune myocarditis are routinely used to investigate the immune mechanisms underlying dilated cardiomyopathy. However, their translational relevance is limited because observations made in a single inbred strain may not reflect those of outbred human populations. This limitation can be overcome by using Diversity Outbred (DO) mice, whose genetic variability is comparable to that of humans. Methods. To investigate the utility of DO mice, we characterized their immune cell distributions and induced myocarditis by immunization with porcine cardiac myosin (PCM) emulsified in complete Freund’s adjuvant. Antigen-specific T cell and antibody responses were evaluated using lymphocytes and serum samples, respectively, and hearts were examined histologically for inflammatory changes. Results. First, we noted no significant variations in the majority of immune cell populations, which include T cells and B cells. However, NK cells, double positive for CD49b and NK1.1, were lacking in both sexes. While we noted sex differences in the expression of major histocompatibility complex class II molecules in antigen-presenting cells, expression of costimulatory molecules was similar in both sexes. Second, upon immunization, we demonstrated that the PCM was immunogenic, and the PCM-reactive T cell responses were generated in both males and females, as measured by a proliferation assay. Third, cytokine analysis revealed marginal detection of Th1 (IFN-γ) and Th17 (IL-17 and IL-22) cytokines, mainly with three doses of immunization. Fourth, determination of PCM-reactive antibody responses revealed significant amounts of IgG1 and IgG2b isotypes. Finally, histological analysis revealed varying degrees of myocarditis in individual mice of both sexes. Conclusions. Our data suggest that mild autoimmune myocarditis can be induced in DO mice. However, to capture the heterogeneity in disease susceptibility, large sample cohorts are required. Full article
(This article belongs to the Special Issue Advances in Cardiac and Vascular Biology: From Mechanisms to Pathophysiology)
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Review

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19 pages, 1655 KB  
Review
From Byproduct to Regulator: The Expanding Role of Lactate and Lactylation in Cardiovascular Physiology and Disease
by Hanqiang Deng
Biology 2026, 15(8), 642; https://doi.org/10.3390/biology15080642 - 18 Apr 2026
Viewed by 810
Abstract
Metabolic reprogramming plays a critical role in the pathogenesis of cardiovascular diseases. Historically regarded as a metabolic waste product, lactate has recently emerged as a critical regulator of vascular biology, exerting both metabolic and signaling functions. Moreover, the discovery of protein lactylation, a [...] Read more.
Metabolic reprogramming plays a critical role in the pathogenesis of cardiovascular diseases. Historically regarded as a metabolic waste product, lactate has recently emerged as a critical regulator of vascular biology, exerting both metabolic and signaling functions. Moreover, the discovery of protein lactylation, a novel post-translational modification derived from lactate, has revealed a direct link between metabolic flux and gene regulation. This review provides a comprehensive overview of the evolving roles of lactate and lactylation in cardiovascular physiology and disease, offering insights into potential therapeutic interventions. It first provides a historical perspective of lactate and lactylation, followed by an overview of lactate metabolism, lactate shuttle theory and signaling pathways. It then discusses the mechanism and regulation of lactylation, focusing on its writers, erasers, and readers. Finally, this review summarizes clinical implications of lactate and lactylation in various cardiovascular diseases, including atherosclerosis, pulmonary hypertension, myocardial infarction, heart failure, and diabetic vascular complications. A deeper understanding of the mechanisms underlying the lactate–lactylation axis may facilitate the development of new therapeutic strategies to prevent or treat cardiovascular diseases. Full article
(This article belongs to the Special Issue Advances in Cardiac and Vascular Biology: From Mechanisms to Pathophysiology)
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16 pages, 1066 KB  
Review
Mesenchymal Stem Cell-Derived Extracellular Vesicles in Myocardial Ischemia–Reperfusion Injury: A Comprehensive Review
by Luca Bonanni and Nicola Ferri
Biology 2026, 15(5), 383; https://doi.org/10.3390/biology15050383 - 26 Feb 2026
Viewed by 882
Abstract
Myocardial ischemia–reperfusion injury remains a major unresolved challenge in cardiovascular medicine. Although timely restoration of blood flow is essential to limit ischemic damage, reperfusion triggers a complex network of maladaptive biological responses, including oxidative stress, calcium overload, mitochondrial dysfunction, metabolic impairment, and sterile [...] Read more.
Myocardial ischemia–reperfusion injury remains a major unresolved challenge in cardiovascular medicine. Although timely restoration of blood flow is essential to limit ischemic damage, reperfusion triggers a complex network of maladaptive biological responses, including oxidative stress, calcium overload, mitochondrial dysfunction, metabolic impairment, and sterile inflammation. These processes converge on cardiomyocyte death, adverse ventricular remodeling, and long-term functional deterioration. Mesenchymal stem cells have been widely investigated as cardioprotective agents; however, accumulating evidence indicates that their beneficial effects are predominantly mediated by paracrine mechanisms. Among these, extracellular vesicles released by mesenchymal stem cells have emerged as key biological effectors. Experimental studies demonstrate that mesenchymal stem cell–derived extracellular vesicles modulate multiple signaling pathways involved in ischemia–reperfusion injury, including activation of the phosphoinositide 3-kinase (PI3K) and protein kinase B (PKB) axis, regulation of signal transducer and activator of transcription 3 (STAT3) signaling in a cell-specific manner, suppression of nuclear factor kappa B (NF-κB)-driven inflammatory responses, and stabilization of hypoxia-inducible factor-1α (HIF-1α)–dependent adaptive programs. At the subcellular level, these vesicles preserve mitochondrial structure and function, support energy metabolism, regulate mitophagy, and limit oxidative damage. Their molecular cargo, comprising regulatory microRNAs, metabolic enzymes, and stress-response proteins, enables coordinated modulation of survival, inflammatory, and reparative pathways rather than single-target effects. This review synthesizes current experimental evidence on the mechanistic basis of mesenchymal stem cell–derived extracellular vesicle–mediated cardioprotection and discusses their potential as cell-free, mechanism-based therapeutic strategies to limit myocardial ischemia–reperfusion injury. Full article
(This article belongs to the Special Issue Advances in Cardiac and Vascular Biology: From Mechanisms to Pathophysiology)
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