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Molecular Mechanism in Cardiovascular Pathology
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Molecular Mechanism in Cardiovascular Pathology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 October 2025 | Viewed by 3105

Special Issue Editor

Dr. Andrea Marzullo

E-Mail Website
Guest Editor
Section of Pathology, Department of Precision and Regenerative Medicine and Ionian Area (DIMEPReJ), University of Bari, 70124 Bari, Italy
Interests: cardiovascular pathology; head and neck diseases; immunohistochemistry; autopsies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Understanding the molecular basis of cardiovascular diseases (CVDs) is crucial for advancing diagnostics, treatment, and prevention strategies. At the heart of these diseases are complex genetic, cellular, and biochemical interactions that regulate heart function and blood vessels. By deciphering these molecular mechanisms, researchers can identify biomarkers for early detection and develop targeted therapies to improve patient outcomes. This knowledge also offers insights into the underlying causes of conditions such as atherosclerosis, heart failure, and many others, paving the way for more personalized and effective medical interventions.

Supervised by Dr. Andrea Marzullo and assisted by Dr. Cecilia Salzillo from University of Campania “Luigi Vanvitelli, this Special Issue focuses on recent studies that aim to investigate the molecular basis of cardiovascular diseases including inflammatory, degenerative, and functional conditions, with a particular interest on sudden death, cardiomyopathies, coronary artery diseases, pericarditis, and heart failure. Submissions of pathological and molecular studies including biomolecular experiments (but not pure clinical experiments) are welcomed to comply with the aim of the journal.

Dr. Andrea Marzullo
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

  • cardiovascular diseases
  • molecular biology
  • sudden death
  • cardiomyopathies
  • heart failure
  • coronary artery diseases
  • pericarditis

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Published Papers (3 papers)

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Research

20 pages, 6445 KiB  
Article
Transcriptome Insights into Protective Mechanisms of Ferroptosis Inhibition in Aortic Dissection
by Chun-Che Shih, Chi-Yu Chen, Chih-Pin Chuu, Chun-Yang Huang, Chia-Jung Lu and Hsin-Ying Lu
Int. J. Mol. Sci. 2025, 26(9), 4338; https://doi.org/10.3390/ijms26094338 - 2 May 2025
Viewed by 105
Abstract
Aortic dissection (AD) is a life-threatening vascular condition with limited pharmacological options, and shared risk factors with cardiac disease include hypertension, atherosclerosis, smoking, and dyslipidemia. This study investigated Ferrostatin-1 (Fer-1), a ferroptosis inhibitor, in a BAPN/Ang-II-induced mouse model of AD, revealing significant therapeutic [...] Read more.
Aortic dissection (AD) is a life-threatening vascular condition with limited pharmacological options, and shared risk factors with cardiac disease include hypertension, atherosclerosis, smoking, and dyslipidemia. This study investigated Ferrostatin-1 (Fer-1), a ferroptosis inhibitor, in a BAPN/Ang-II-induced mouse model of AD, revealing significant therapeutic potential. Fer-1 significantly reduced AD incidence and mortality by preserving aortic wall integrity. RNA sequencing identified 922 differentially expressed genes, with 416 upregulated and 506 downregulated. Bioinformatics analysis revealed that Fer-1 modulates key regulators, such as MEF2C and KDM5A, impacting immune responses, oxidative stress, apoptosis, and lipid metabolism. Additionally, Fer-1 alters miRNA expression, with the upregulation of miR-361-5p and downregulation of miR-3151-5p, targeting pathways involved in inflammation, oxidative stress, and smooth muscle cell (SMC) phenotypic stability. Functional pathway analysis highlighted the inhibition of actin cytoskeleton, ILK, and IL-17 signaling, essential for SMC differentiation and extracellular matrix remodeling. Gene interaction network analysis identified 21 central molecules, including CXCR3, ACACA, and BPGM, associated with lipid metabolism, inflammation, and vascular remodeling. This research elucidates the mechanism of ferroptosis in AD pathogenesis and establishes Fer-1 as a promising therapeutic intervention. AD and cardiac diseases share molecular mechanisms, risk factors, and pathological processes, positioning AD within the broader scope of cardiovascular pathology. By attenuating lipid peroxidation, oxidative stress, and inflammation, Fer-1 may have cardioprotective effects beyond AD, providing a foundation for future translational research in cardiovascular medicine. Full article
(This article belongs to the Special Issue Molecular Mechanism in Cardiovascular Pathology)
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13 pages, 11901 KiB  
Article
Spatial Gene Expression of Human Coronary Arteries Revealed the Molecular Features of Diffuse Intimal Thickening in Explanted Hearts
by Boaz Li, Samuel Leung, Maria Elishaev, Wan Hei Cheng, Giuseppe Mocci, Johan L. M. Björkegren, Chi Lai, Amrit Singh and Ying Wang
Int. J. Mol. Sci. 2025, 26(5), 1949; https://doi.org/10.3390/ijms26051949 - 24 Feb 2025
Viewed by 1857
Abstract
Diffuse intimal thickening (DIT) is a pre-clinical stage of atherosclerosis characterized by thickened intima. The molecular basis of its susceptibility to atherogenesis is unknown, and mechanistic investigations cannot be performed in commonly used mouse models, in which DIT does not exist. Vascular smooth [...] Read more.
Diffuse intimal thickening (DIT) is a pre-clinical stage of atherosclerosis characterized by thickened intima. The molecular basis of its susceptibility to atherogenesis is unknown, and mechanistic investigations cannot be performed in commonly used mouse models, in which DIT does not exist. Vascular smooth muscle cells (SMCs) are the predominant cell type that occupies the intima and media of DIT. The molecular differences between these two layers may reveal the earliest phenotypic changes in SMCs to promote atherosclerosis. We benchmarked the RNA quality of human coronary arteries from autopsies (n = 7) and explanted hearts (n = 7) and performed Visium spatial gene expression on tissue sections with DIT. Although autopsy samples met the RNA quality standard for Visium (DV200 ≥ 30%), only arteries from explanted hearts exhibited reliable sequencing performance. Genes enriched in TGF-β-mediated remodeling of the extracellular matrix were overrepresented in the intima. SMCs enriched in the intima are dedifferentiated, but unlike those in the atherosclerotic lesions, they are not pro-inflammatory. Our findings indicate that autopsy samples are not ideal to distinguish subtle differences among cell phenotypes. SMCs in thickened intima may lead to lipid retention but not necessarily the onset of atherosclerosis. Full article
(This article belongs to the Special Issue Molecular Mechanism in Cardiovascular Pathology)
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15 pages, 3614 KiB  
Article
Different Gut Microbiome Profiles in Patients with Transthyretin Amyloidosis with and Without Cardiac Involvement
by João Henrique Rissato, Natalia de Melo Pereira, Cristhian Espinoza Romero, Georgina del Cisne Jadán Luzuriaga, Bruno Vaz Kerges Bueno, Caio Rebouças Fonseca Cafezeiro, Aristóteles Comte de Alencar Neto, Thaís Sousa Borges, Suenia Freitas Carvalhal, Félix Jose Alvarez Ramires, Luciano Nastari, Charles Mady and Fábio Fernandes
Int. J. Mol. Sci. 2025, 26(4), 1689; https://doi.org/10.3390/ijms26041689 - 16 Feb 2025
Viewed by 591
Abstract
Transthyretin amyloidosis (ATTR amyloidosis) is characterized by the buildup of amyloid protein in organs like the gut and the heart. As a result, hypoperfusion, edema, and dysautonomia cause an imbalance in the gut microbiome. We aimed to identify the gut microbiome composition in [...] Read more.
Transthyretin amyloidosis (ATTR amyloidosis) is characterized by the buildup of amyloid protein in organs like the gut and the heart. As a result, hypoperfusion, edema, and dysautonomia cause an imbalance in the gut microbiome. We aimed to identify the gut microbiome composition in ATTR amyloidosis patients with and without heart involvement, as well in controls. Sixty participants were divided into three groups: 20 with ATTR amyloidosis and heart involvement (G1), 19 with ATTR amyloidosis but no heart disease (G2), and 21 controls (G3). The microbiome profiles were obtained through 16S rRNA gene sequencing. Additional evaluations included a clinical questionnaire, echocardiogram, six-minute walk tests, troponin, BNP, and genotype analysis. Compared to G3, G1, and G2 groups had different levels of Streptococcus, Lachnospiraceae, and Sellimonas, while the controls showed a higher relative abundance of Methanosphaera. Streptococcus was linked to higher troponin levels. Lachnospiraceae was associated with lower BNP levels and smaller left atrium volumes. Sellimonas was associated with a higher intestinal symptom score, while Methanosphaera with a lower symptom score. ATTR amyloidosis patients have a different intestinal microbiome profile compared to the control group. There were correlations with genotype, gastrointestinal symptoms, heart failure biomarkers, echocardiographic parameters, and the six-minute walk test. Full article
(This article belongs to the Special Issue Molecular Mechanism in Cardiovascular Pathology)
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