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Metabolic Dysfunction and Cardiovascular Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (31 March 2026) | Viewed by 390

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Clinical and Molecular Medicine Department, Faculty of Medicine and Psychology, Sant’Andrea Hospital, Sapienza University of Rome, 00189 Rome, Italy
Interests: cardiology; cardiovascular diseases
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Special Issue Information

Dear Colleague,

Metabolic dysfunction is increasingly recognized as a central driver of cardiovascular disease (CVD), contributing to its global burden of morbidity and mortality. Obesity, insulin resistance, dyslipidemia, and type 2 diabetes mellitus create a complex pathophysiological milieu that promotes vascular injury, myocardial remodeling, arrhythmogenesis, and accelerated atherosclerosis. The interplay between metabolic derangements and cardiovascular pathology is mediated by multiple molecular and cellular mechanisms, including oxidative stress, chronic low-grade inflammation, endothelial dysfunction, mitochondrial impairment, maladaptive immune responses, and altered substrate utilization. Genetic and epigenetic determinants, together with non-coding RNAs, further shape disease susceptibility and progression. Despite advances in pharmacological and interventional therapies, the mechanistic links between metabolic dysfunction and CVD have not yet been fully elucidated, hampering the development of precision medicine approaches. 

This Special Issue of the International Journal of Molecular Sciences will highlight cutting-edge research into molecular pathways, biomarkers, and translational strategies connecting metabolic dysfunction and cardiovascular disease. By fostering interdisciplinary contributions, we aim to promote mechanistic understanding and accelerate innovation in prevention, diagnosis, and treatment.

Prof. Dr. Carmine Savoia
Guest Editor

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Keywords

  • metabolic dysfunction
  • cardiovascular disease
  • inflammation
  • endothelial dysfunction
  • oxidative stress
  • biomarkers

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Published Papers (1 paper)

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Research

16 pages, 6026 KB  
Article
The Progression of Cardiac Damage in the Offspring of Mothers with Gestational Diabetes Is Regulated by the p53/miR-34/SIRT1/7 Pathway
by Guadalupe Díaz-Rosas, Omar Gómez-Acuña, Renata Saucedo, Ricardo Chávez-García, Alfonso Reyes-López, Alejandra Contreras-Ramos and Clara Ortega-Camarillo
Int. J. Mol. Sci. 2026, 27(10), 4368; https://doi.org/10.3390/ijms27104368 - 14 May 2026
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Abstract
Gestational diabetes mellitus (GDM) exposes the fetus to chronic hyperglycemia, promoting early cardiac remodeling and increasing the risk of diabetic cardiomyopathy later in life. Epigenetic regulators such as p53 tumor suppressor gene (p53), microRNA-34a (miR-34a), and the sirtuins 1 [...] Read more.
Gestational diabetes mellitus (GDM) exposes the fetus to chronic hyperglycemia, promoting early cardiac remodeling and increasing the risk of diabetic cardiomyopathy later in life. Epigenetic regulators such as p53 tumor suppressor gene (p53), microRNA-34a (miR-34a), and the sirtuins 1 and 7 (SIRT1/SIRT7) may contribute to this programming process; however, their temporal dynamics during postnatal cardiac development remain unclear. This study aimed to characterize structural and molecular alterations in the hearts of offspring exposed to GDM and to determine the involvement of the p53miR-34a–SIRT1/SIRT7 axis in early cardiac remodeling. Cardiac morphometry was assessed at birth (newborn [NB]) and at 8, 15, 25, and 35 days. Left ventricles were examined through hematoxylin/eosin staining. SIRT1, SIRT7, Bcl-2, and Bax were evaluated by immunofluorescence, while p53 and miR-34a were evaluated by RT-PCR. Molecular interactions were integrated using IPA software, version 159584291. Offspring exposed to GDM exhibited a reduced cardiac area and ventricular lumen, along with increased left ventricular wall thickness and fibrosis during early postnatal stages. The cardiomyocyte area was elevated at all ages. The level of miR-34a increased early, preceding p53 upregulation. SIRT1 presences decreased from NB to 35 days, whereas SIRT7 expression remained consistently elevated. These findings suggest that GDM induces early and sustained cardiac remodeling associated with dysregulation of the p53–miR-34a–SIRT1/SIRT7 axis, a pattern that could increase susceptibility to diabetic cardiomyopathy. Full article
(This article belongs to the Special Issue Metabolic Dysfunction and Cardiovascular Disease)
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