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Cellular and Molecular Mechanisms of Cardiovascular and Metabolic Diseases, 3rd Edition

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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: 30 October 2026 | Viewed by 3712

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Editor

Dr. Paramjit S. Tappia

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Guest Editor

Asper Clinical Research Institute, St. Boniface Hospital, Winnipeg, MB R2H 2A6, Canada
Interests: cardiovascular disease; diabetes; nutrition; early-stage lung cancer
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Special Issue Information

Dear Colleagues,

Cardiovascular and metabolic diseases, including obesity and diabetes, are major global health hazards that also represent increasing human and economic burdens. However, the underlying cellular and molecular processes that cause these abnormalities are not fully understood. Therefore, a complete understanding of the cellular and molecular mechanisms involved in the development of cardiovascular and metabolic diseases could help in the introduction of novel strategies for an improved reduction in the risk/predisposition of such diseases in vulnerable and at-risk populations, as well as better-quality treatment. It is envisioned that this Special Issue will bring together contributions from experts around the world to describe recent advances in the different mechanisms that lead to the development of cardiovascular and metabolic diseases. This Special Issue will be uniquely positioned, as it will focus on the cellular and molecular mechanisms of cardiovascular disease as well as metabolic diseases including obesity and diabetes. Since cardiovascular and metabolic diseases are linked and can occur concomitantly, an interplay or overlapping of some mechanisms may exist between these pathophysiological conditions, which may be of scientific interest. Overall, the information provided in this Special Issue will be of value in the design of novel therapeutic interventions to reduce or reverse cardiovascular and metabolic diseases, as well as assist in establishing improved approaches for their prevention.

Dr. Paramjit S. Tappia
Guest Editor

Manuscript Submission Information

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Keywords

cardiovascular diseases
metabolic diseases
cellular and molecular mechanisms

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Published Papers (6 papers)

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Research

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16 pages, 23858 KB

Open AccessArticle

Cross-Species Identification and Validation of Hub Genes and Potential Therapeutic Targets in Myocardial Infarction

by Zhiyong Sheng, Qiang Li, Mingyu Bao, Wenjing Wang, Zitong Chen and Jiali Guo

Int. J. Mol. Sci. 2026, 27(13), 6050; https://doi.org/10.3390/ijms27136050 - 6 Jul 2026

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Abstract

Myocardial infarction (MI) is a leading cause of mortality worldwide. Identification of robust and translatable molecular markers remains challenging due to inter-dataset and inter-species variability. In this study, we performed a cross-species integrative analysis to identify conserved hub genes and potential therapeutic targets in MI. Analysis revealed five hub genes (IL6, SERPINE1, MMP14, PLAUR, and ENO1), which were consistently validated across human peripheral blood and multiple animal models. A multigene diagnostic model demonstrated strong predictive performance (AUC = 0.904). The model was developed to distinguish myocardial infarction (MI) samples from non-MI control samples in an independent peripheral blood dataset. Drug–gene interaction analysis identified candidate therapeutic compounds. These results are computational predictions from the DGIdb database and do not represent validated therapeutic effects in myocardial infarction. These findings highlight conserved molecular mechanisms of MI and provide potential biomarkers and therapeutic targets with translational relevance. Full article

(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Cardiovascular and Metabolic Diseases, 3rd Edition)

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14 pages, 11430 KB

Open AccessArticle

Mechanistic Role of Sestrin2 in Exercise-Mediated Cardioprotection Against Obesity-Related Cardiomyopathy

by Meili Hao, Wanyu Zhu, Li Zhao and Wenyan Bo

Int. J. Mol. Sci. 2026, 27(13), 5670; https://doi.org/10.3390/ijms27135670 - 23 Jun 2026

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Abstract

Exercise is one of the safe and effective methods to improve obesity and its complications, but the mechanism has not been fully elucidated. Sestrin2 (SESN2) is a stress-induced protein that protects cells from stress damage. The role and mechanism of SESN2 in the improvement of obesity-induced cardiac dysfunction by exercise are still unclear. Male C57BL/6J mice were used to prepare a high-fat diet-induced obesity mouse model and conducted aerobic exercise training. After training, echocardiography was used to evaluate the cardiac function of mice, and HE and Masson staining were used to assess the extent of cardiac damage. Cell experiments were conducted using the H9C2 cell line derived from embryonic rat hearts, with the intervention of palmitic acid ester and exogenous SESN2. We detected indicators related to myocardial cell damage, fibrosis, inflammation, and oxidative stress, as well as the activation level of the AMPK-PGC-1α signaling pathway. The results showed that aerobic exercise significantly inhibited myocardial fibrosis, inflammation, oxidative stress, and cell damage in HFD mice, upregulated cardiac SESN2 expression, and activated the AMPK-PGC-1α signaling pathway. Cell experiments have found that exogenous SESN2 pretreatment alleviates palmitate-induced injury, inflammation, and oxidative stress in H9C2 cardiomyocytes, and activates the AMPK-PGC-1α signaling pathway. This indicates that aerobic exercise significantly upregulates the expression of SESN2 and activates the AMPK-PGC-1α signaling pathway, which is potentially involved in alleviating myocardial inflammation, oxidative stress, cardiac fibrosis and cardiac dysfunction in HFD mice. Full article

(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Cardiovascular and Metabolic Diseases, 3rd Edition)

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20 pages, 1596 KB

Open AccessArticle

Amino Acid-Derived Metabolic Signature Across Stages of Systolic Dysfunction: Derivation and Internal Evaluation of the HASI (Heart Failure Amino Acid-Derived Systolic Index)—40 Index

by Beata Krasińska, Ievgen Spasenenko, Dagmara Pietkiewicz, Szymon Plewa, Krzysztof J. Filipiak, Katarzyna Pawlaczyk-Gabriel, Jarosław Bartkowski, Andrzej Tykarski, Zbigniew Krasiński, Jan Matysiak and Tomasz Urbanowicz

Int. J. Mol. Sci. 2026, 27(10), 4459; https://doi.org/10.3390/ijms27104459 - 15 May 2026

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Abstract

Heart failure with reduced ejection fraction (HFrEF) is increasingly recognized as a systemic metabolic disorder. The aim of this study was to characterize amino acid-related metabolic differences between heart failure with moderately reduced ejection fraction (HFmrEF) (LVEF 40–49%) and HFrEF (LVEF < 40%) and to derive a biologically interpretable composite metabolomic index capable of discriminating between these two stages of systolic dysfunction. We conducted a cross-sectional metabolomic analysis of 42 patients stratified by left ventricular ejection fraction (LVEF < 40% vs. 40–49%). The reference group comprised patients with mildly reduced ejection fraction (LVEF 40–49%), without inclusion of individuals with preserved or normal cardiac function. Targeted amino acid profiling was performed using liquid chromatography-tandem mass spectrometry (LC–MS/MS). Metabolites were standardized and analyzed individually and in combination. A composite index (Heart Failure Amino Acid-Derived Systolic Index: HASI-40), integrating markers of proteolysis and metabolic resilience, was derived to distinguish patients with HFrEF from those with HFmrEF. Discrimination was assessed using receiver operator curve (ROC) analysis with internal validation and multivariable adjustment. Patients with LVEF < 40% exhibited a coordinated metabolic phenotype characterized by reduced methionine, sarcosine, serine, and taurine. While individual metabolites did not retain significance after multiple-testing correction, the composite HASI-40 index remained strongly associated with HFrEF (OR 5.56, 95% CI: 1.70–18.14; p = 0.004), although the wide confidence interval indicates limited precision due to sample size. The index demonstrated good discrimination with an area under the curve (AUC) of 0.862, which improved when combined with age (AUC 0.932). The index represents a standardized composite measure and does not define a diagnostic cutoff for individual patients. These findings suggest that HFmrEF and HFrEF exhibit partially distinct metabolic phenotypes despite overlapping clinical characteristics. These findings suggest that HASI-40 captures metabolic differences between patients with HFmrEF (LVEF 40–49%) and those with HFrEF (LVEF < 40%), reflecting progression toward more advanced systolic dysfunction. However, due to the absence of a control group with preserved ejection fraction, small sample size, and lack of external validation, the index should be considered exploratory and hypothesis-generating rather than clinically applicable. Full article

(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Cardiovascular and Metabolic Diseases, 3rd Edition)

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Review

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29 pages, 814 KB

Open AccessReview

The Impact of Risk Factors and Comorbidities on Heart Failure in the Aging Population

by Ruzzell C. Flores, Fatin Shadab Talukder and Inna Rabinovich-Nikitin

Int. J. Mol. Sci. 2026, 27(12), 5296; https://doi.org/10.3390/ijms27125296 - 11 Jun 2026

Cited by 1 | Viewed by 650 | Correction

Abstract

Heart failure (HF) represents a major and escalating public health challenge in the aging population. Older adults with HF frequently present with coexisting conditions such as hypertension, diabetes mellitus and obesity, which substantially influence disease pathophysiology, clinical presentation, therapeutic response and prognosis. The complex interplay between HF risk factors and comorbidities complicates diagnosis, limits the applicability of guideline-directed therapies and contributes to increased symptom burden, recurrent hospitalizations, higher healthcare utilization and reduced quality of life. In this Review, we examine the mechanisms through which common risk factors and comorbidities modify HF progression and outcomes in elderly patients, highlighting their impact on disease severity and treatment effectiveness. We emphasize the need for individualized, patient-centered management strategies that move beyond a single-disease framework and incorporate multidisciplinary care models. Early identification of comorbidities tailored pharmacological and non-pharmacological interventions, and longitudinal monitoring are essential to address the dual burden of HF and multimorbidity. Finally, we discuss current knowledge gaps and future research priorities, including the need to elucidate shared pathophysiological pathways and to develop integrated therapeutic approaches. Advancing our understanding of HF in the context of aging and risk factor/comorbidity is critical for improving clinical outcomes and informing healthcare policy in this growing patient population. Full article

(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Cardiovascular and Metabolic Diseases, 3rd Edition)

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46 pages, 1064 KB

Open AccessReview

Vasculoprotective Effects of Sodium-Glucose Co-Transporter Inhibitors in Non-Diabetic Experimental Settings: A Narrative Review

by Darius G. Buriman, Lavinia Noveanu, Adina V. Furdui-Lința, Horea B. Feier, Antigone Lazou, Attila Kiss, Bruno K. Podesser, Maria D. Dănilă, Adrian Sturza and Danina M. Muntean

Int. J. Mol. Sci. 2026, 27(6), 2573; https://doi.org/10.3390/ijms27062573 - 11 Mar 2026

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Abstract

Sodium-glucose co-transporter (SGLT) inhibitors are a novel class of glucose-lowering drugs with beneficial pleiotropic effects that have been widely investigated in the past decade in several experimental models and patients in the absence of diabetes. There are two types of transporters: the SGLT1 isoform that is distributed across a broad range of tissues, including the cardiovascular system, and the SGLT2 isoform, which is mostly expressed in renal proximal tubular cells. It is known that inflammation and oxidative stress are key contributors to vascular damage and the progression of atherosclerosis. SGLT inhibitors have demonstrated multiple benefits that contribute to improved vascular health, including alleviation of endothelial function, anti-inflammatory and antioxidative effects, and mitigation of arterial stiffness, all contributing to blood pressure decrease. An increasing body of research has tackled the molecular and cellular mechanisms of their chronic and, more recently, acute cardiovascular beneficial effects. This narrative review specifically delves into the direct vasculoprotective effects of SGLT2 and dual SGLT1/2 inhibitors, summarizing their off-target mechanisms described in various experimental settings (animal models, animal and human cell lines/samples). Full article

(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Cardiovascular and Metabolic Diseases, 3rd Edition)

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