ijms-logo

Journal Browser

Journal Browser

Metabolic Crossroads in Cardiac Pathophysiology

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: closed (20 June 2026) | Viewed by 1102

Editor


E-Mail Website
Guest Editor
Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
Interests: internal medicine; cardiovascular disease; electrophysiology

Special Issue Information

Dear Colleagues,

Cardiovascular disease remains the leading global cause of morbidity and mortality, yet its underlying pathophysiology is increasingly recognized as a convergence of metabolic, inflammatory, and hemodynamic dysfunction. This Special Issue, "Metabolic Crossroads in Cardiac Pathophysiology", invites original research articles, reviews, and translational perspectives that explore how metabolic perturbations drive cardiac remodeling, heart failure, ischemia–reperfusion injury, arrhythmogenesis, and vascular dysfunction.

We are particularly interested in submissions that examine the interface between cardiac energetics and systemic metabolic disorders—such as diabetes, obesity, insulin resistance, dyslipidemia, and chronic kidney disease—as well as investigations into mitochondrial function, substrate utilization, oxidative stress, nutrient signaling pathways, and the role of emerging cardiometabolic therapies (e.g., SGLT2 inhibitors, GLP-1 receptor agonists, and novel peptide-based interventions).

This Special Issue aims to highlight the evolving paradigm in which cardiac disease is viewed not solely as a mechanical or electrical failure, but as a metabolic syndrome of the heart. We welcome interdisciplinary work spanning basic science, omics-based discovery, clinical trials, imaging, and bioengineering, especially where novel mechanisms or therapeutic targets are identified.

We encourage authors from across cardiovascular science, endocrinology, nephrology, and metabolism to contribute their work and help shape this timely and transformative discourse.

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

  • Cardiac metabolism in heart failure with preserved or reduced ejection fraction (HFpEF/HFrEF);
  • Myocardial insulin resistance and lipid overload;
  • Metabolomic and proteomic profiling in cardiometabolic disease;
  • Endothelial and glycocalyx dysfunction in metabolic states;
  • Mitochondrial energetics and redox imbalance in ischemic heart disease;
  • Novel pharmacologic and non-pharmacologic metabolic interventions;
  • Gut microbiota, TMAO, and metabolic inflammation in CVD;
  • Chronobiology and metabolic regulation of cardiac function.

Join us in advancing the understanding of how metabolic networks intersect with cardiac pathophysiology and in identifying new avenues for therapeutic innovation.

Prof. Dr. Robert J. Chilton
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 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-anonymized 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

  • cardiometabolic disease
  • cardiac metabolism
  • heart failure
  • mitochondrial dysfunction
  • insulin resistance
  • cardiometabolic therapies
  • metabolomics

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

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

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

15 pages, 1873 KB  
Article
Phosphatidylinositol 4-Kinase IIIβ: A Therapeutic Target for Contractile Dysfunction in Hypertrophic Cardiomyocytes
by Myrthe M. A. Willemars, Aomin Sun, Shujin Wang, Ozlenen Simsek Papur, Agnieszka Brouns-Strzelecka, Rick van Leeuwen, Sabina J. V. Vanherle, Dimitrios Kapsokalyvas, Jan F. C. Glatz, Dietbert Neumann, Miranda Nabben and Joost J. F. P. Luiken
Int. J. Mol. Sci. 2026, 27(2), 595; https://doi.org/10.3390/ijms27020595 - 7 Jan 2026
Viewed by 779
Abstract
Cardiac hypertrophy is an important risk factor for heart failure and is often accompanied by contractile dysfunction. While hypertrophic growth contributes to disease progression, the underlying molecular mechanisms remain incompletely understood. A proposed contributor is a metabolic shift toward glucose uptake, suggesting that [...] Read more.
Cardiac hypertrophy is an important risk factor for heart failure and is often accompanied by contractile dysfunction. While hypertrophic growth contributes to disease progression, the underlying molecular mechanisms remain incompletely understood. A proposed contributor is a metabolic shift toward glucose uptake, suggesting that kinases regulating this process, such as protein kinase D1 (PKD1) and downstream target phosphatidylinositol 4-kinase IIIβ (PI4KIIIβ), might be effective targets to mitigate cardiac hypertrophy-induced contractile dysfunction. We investigated whether PI4KIIIβ inhibition downregulates enhanced glucose uptake in hypertrophic cardiomyocytes and thereby treats cardiac hypertrophy-induced contractile dysfunction. Hypertrophy was induced in cultured adult rat cardiomyocytes and human stem cell-derived cardiomyocytes using either phenylephrine (PE) or adenoviral PKD1 overexpression. PE-induced hypertrophy was associated with increased mRNA expression of BNP, activation of hypertrophic signaling, morphological alterations, enhanced protein synthesis and glucose uptake, and impaired contractile function. Treatment with the PI4KIIIβ inhibitor MI14 prevented and reversed PE-stimulated glucose uptake and contractile dysfunction, while hypertrophic signaling, cell size, and protein synthesis remained unaffected. Similar effects on glucose uptake were observed in the PKD1 overexpression model. These findings suggest that targeting myocardial substrate metabolism via the PI4KIIIβ pathway, rather than hypertrophic growth itself, could be a promising strategy to treat hypertrophy-induced contractile dysfunction. Full article
(This article belongs to the Special Issue Metabolic Crossroads in Cardiac Pathophysiology)
Show Figures

Graphical abstract

Back to TopTop