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Metabolic Alterations in Health and Disease: From Molecular Mechanisms to Biomarkers in Clinical Applications

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 7123

Editors

Dr. Ramona D'Amico

E-Mail Website
Guest Editor
Department of Medicine and Surgery, University of Enna Kore, 94100 Enna, Italy
Interests: oxidative stress; inflammation; metabolic disorders; diabetes; molecular and cellular mechanisms; biomarkers; bioactive compounds
Special Issues, Collections and Topics in MDPI journals
Dr. Rosalba Siracusa

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy
Interests: clinical biochemistry; molecular biology; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic alterations represent a key hallmark of numerous pathological conditions, ranging from cancer and neurodegenerative diseases to cardiovascular and metabolic disorders. Changes in metabolic pathways influence energy balance, biosynthesis, and redox regulation, ultimately affecting cell growth, differentiation, and survival. When metabolic regulation is disrupted, cells may undergo profound functional and structural changes that impact overall organismal health. Understanding the molecular mechanisms driving these metabolic changes is crucial for identifying novel diagnostic biomarkers and therapeutic targets. This Special Issue aims to highlight recent discoveries in the molecular mechanisms underlying metabolic alterations and their systemic consequences. We welcome various types of manuscripts, including original research and comprehensive reviews. Studies employing integrative and translational approaches that bridge basic molecular research with clinical implications are particularly encouraged.

We look forward to receiving your contributions.

Dr. Ramona D'Amico
Dr. Rosalba Siracusa
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-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

  • metabolic syndrome
  • diabetes
  • oxidative stress
  • cellular metabolism
  • biomarkers
  • molecular pathways
  • metabolic disorders

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Published Papers (6 papers)

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Research

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21 pages, 2091 KB  
Article
Visceral Adiposity Is Associated with Elevated Interleukin-1 Receptor Antagonist Levels and Anxiety Symptoms in Schizophrenia
by Aleksandra Julia Oracz, Stefan Modzelewski, Mateusz Zwierz, Maria Suprunowicz, Joanna Matowicka-Karna and Napoleon Waszkiewicz
Int. J. Mol. Sci. 2026, 27(14), 6351; https://doi.org/10.3390/ijms27146351 - 17 Jul 2026
Viewed by 378
Abstract
Schizophrenia spectrum disorders are associated with visceral obesity and chronic low-grade inflammation. However, the role of inflammatory mediators in anxiety and depressive symptoms remains unclear. This study aimed to investigate associations between body fat distribution, circulating inflammatory mediators, and affective symptoms in schizophrenia. [...] Read more.
Schizophrenia spectrum disorders are associated with visceral obesity and chronic low-grade inflammation. However, the role of inflammatory mediators in anxiety and depressive symptoms remains unclear. This study aimed to investigate associations between body fat distribution, circulating inflammatory mediators, and affective symptoms in schizophrenia. In this cross-sectional study, 67 patients with schizophrenia were assessed using the Positive and Negative Syndrome Scale (PANSS), with anxiety (G2) and depression (G6) items analyzed separately. Body composition, including visceral fat area (VFA), percent body fat (PBF), and skeletal muscle mass (SMM), was measured using bioelectrical impedance analysis. Serum concentrations of 38 immune mediators were determined using Multiplex technology. Multivariable regression analyses were performed to identify predictors of affective symptoms. Among all analyzed immune mediators, only interleukin-1 receptor antagonist (IL-1ra) was consistently associated with adiposity measures, showing the strongest correlation with VFA (rho = 0.53; p < 0.001). Higher VFA was independently associated with greater anxiety severity (β = 0.32; p = 0.017), whereas depressive symptom severity was associated with higher PBF (β = 0.32) and younger age (β = −0.25). Visceral adiposity was associated with anxiety severity in schizophrenia and may represent a potential marker warranting further investigation. The observed association between IL-1ra and adiposity supports a potential immunometabolic link between metabolic status and affective symptoms in this population. Full article
(This article belongs to the Special Issue Metabolic Alterations in Health and Disease: From Molecular Mechanisms to Biomarkers in Clinical Applications)
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Review

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23 pages, 1797 KB  
Review
Sirtuins at the Interface of Glucose Metabolism, Diabetes, and Heart Failure: Metabolic Sensing in Cardiometabolic Disease
by Jan Krekora, Jarosław Drożdż, Elzbieta Pawlowska and Janusz Blasiak
Int. J. Mol. Sci. 2026, 27(13), 5780; https://doi.org/10.3390/ijms27135780 - 26 Jun 2026
Viewed by 389
Abstract
Heart failure (HF) in the setting of diabetes represents a distinct cardiometabolic phenotype characterized by profound disturbances in myocardial glucose metabolism, mitochondrial function, and energetic efficiency. Growing evidence indicates that sirtuins, a family of nicotinamide adenine dinucleotide (NAD+)-dependent deacylases, play a [...] Read more.
Heart failure (HF) in the setting of diabetes represents a distinct cardiometabolic phenotype characterized by profound disturbances in myocardial glucose metabolism, mitochondrial function, and energetic efficiency. Growing evidence indicates that sirtuins, a family of nicotinamide adenine dinucleotide (NAD+)-dependent deacylases, play a central role in coordinating glucose utilization, oxidative metabolism, and stress responses in the heart. Findings from genetically modified animal models and cardiomyocyte studies demonstrate that sirtuin impairment, often driven by NAD+ depletion and redox imbalance, further suppresses metabolic activity and promotes metabolic inflexibility, whereas restoration of NAD+ availability or sirtuin activity improves mitochondrial efficiency and metabolic coordination. Human studies, including analyses of myocardial tissue and circulating biomarkers, provide supportive but largely associative evidence, highlighting a substantial translational gap. In this review, we synthesize experimental and clinical data linking sirtuin signaling to the metabolic remodeling observed in diabetic HF, with particular emphasis on glycolysis–oxidation uncoupling, pyruvate dehydrogenase regulation, and mitochondrial dysfunction. We critically discuss context-dependent effects, apparent contradictions, and current limitations of the field, emphasizing differences between diabetic and non-diabetic HF, as well as phenotype- and stage-specific considerations. Finally, we explore therapeutic implications and outstanding questions, positioning the NAD+–sirtuin axis as a unifying mechanistic framework that links systemic metabolic disease to cardiac energetic failure and underscores the potential for metabolism-informed, precision strategies in diabetic HF. Full article
(This article belongs to the Special Issue Metabolic Alterations in Health and Disease: From Molecular Mechanisms to Biomarkers in Clinical Applications)
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17 pages, 1642 KB  
Review
The Glutamate–Glutamine Axis in Pediatric Septic Shock: Immunometabolic Mechanisms, Biomarker Potential, and Clinical Implications
by Yaru Cui, Juan Wang and Yiyao Bao
Int. J. Mol. Sci. 2026, 27(11), 4708; https://doi.org/10.3390/ijms27114708 - 23 May 2026
Viewed by 635
Abstract
Pediatric septic shock remains a major cause of morbidity and mortality in critically ill children and is increasingly recognized as a syndrome of profound immunometabolic dysregulation. This narrative review synthesizes current clinical, translational, and mechanistic evidence on the glutamate–glutamine axis in pediatric septic [...] Read more.
Pediatric septic shock remains a major cause of morbidity and mortality in critically ill children and is increasingly recognized as a syndrome of profound immunometabolic dysregulation. This narrative review synthesizes current clinical, translational, and mechanistic evidence on the glutamate–glutamine axis in pediatric septic shock. The review focuses on how glutamine and glutamate metabolism may interact with immune-cell function, mitochondrial substrate handling, redox defense, and intestinal barrier integrity, while distinguishing biological plausibility from validated clinical utility. Current evidence supports the glutamate–glutamine axis as a mechanistically relevant pathway and a source of candidate biomarkers, but pediatric-specific data remain limited and do not yet justify routine biomarker use or glutamine-based intervention in unselected children with septic shock. Future studies should use standardized sampling, reproducible analytical methods, pediatric validation cohorts, and phenotype-guided trial designs before this axis can be translated into clinical decision making. Full article
(This article belongs to the Special Issue Metabolic Alterations in Health and Disease: From Molecular Mechanisms to Biomarkers in Clinical Applications)
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19 pages, 1540 KB  
Review
Monitoring and Targeted Regulation of Oxygen Metabolism in Pediatric Sepsis: Current Paradigms and Future Perspectives
by Hong Zheng, Lijun Guan and Yiyao Bao
Int. J. Mol. Sci. 2026, 27(10), 4454; https://doi.org/10.3390/ijms27104454 - 15 May 2026
Viewed by 488
Abstract
Pediatric sepsis is a life-threatening systemic infectious response syndrome. Its core pathophysiological process involves a systemic imbalance between oxygen delivery and demand, coupled with cellular energy metabolism dysfunction, which collectively contribute to high mortality rates. Parameters of oxygen metabolism serve as critical indicators [...] Read more.
Pediatric sepsis is a life-threatening systemic infectious response syndrome. Its core pathophysiological process involves a systemic imbalance between oxygen delivery and demand, coupled with cellular energy metabolism dysfunction, which collectively contribute to high mortality rates. Parameters of oxygen metabolism serve as critical indicators reflecting tissue perfusion and cellular oxygen utilization. Consequently, these parameters hold significant value for the early identification, severity stratification, therapeutic guidance, and prognostic evaluation of pediatric sepsis. This review systematically elucidates the pathophysiological mechanisms underlying oxygen metabolism disorders in pediatric sepsis. Furthermore, it highlights the current clinical applications and significance of key monitoring indices, including blood lactate, central venous oxygen saturation, oxygen delivery, and oxygen consumption. By integrating recent research advancements, this paper also explores therapeutic strategies aimed at optimizing oxygen metabolism, such as blood purification, microcirculation-targeted therapies, and extracorporeal membrane oxygenation. Finally, we provide future perspectives on emerging biomarkers and metabolomic approaches, aiming to establish a theoretical foundation for the optimized clinical management of pediatric sepsis. Full article
(This article belongs to the Special Issue Metabolic Alterations in Health and Disease: From Molecular Mechanisms to Biomarkers in Clinical Applications)
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20 pages, 521 KB  
Review
Current and Emerging Pharmacological Therapies for Hypertriglyceridemia
by Ibrahim S. Alhomoud
Int. J. Mol. Sci. 2026, 27(8), 3573; https://doi.org/10.3390/ijms27083573 - 16 Apr 2026
Viewed by 2329
Abstract
Hypertriglyceridemia is a well-recognized contributor to residual atherosclerotic cardiovascular disease risk and a predisposing factor for acute pancreatitis. Despite the availability of pharmacologic agents and lifestyle interventions, patients with severe and refractory hypertriglyceridemia often fail to achieve adequate control. Recent advances in the [...] Read more.
Hypertriglyceridemia is a well-recognized contributor to residual atherosclerotic cardiovascular disease risk and a predisposing factor for acute pancreatitis. Despite the availability of pharmacologic agents and lifestyle interventions, patients with severe and refractory hypertriglyceridemia often fail to achieve adequate control. Recent advances in the molecular understanding of triglyceride metabolism have driven the development of targeted therapies that selectively modulate key regulatory pathways. This study sought to provide an overview of triglyceride regulation, the atherogenic role of remnant lipoproteins, and clinical evidence of emerging triglyceride-lowering therapies. Lipoprotein metabolism is regulated by a complex network of regulatory proteins that include lipoprotein lipase (LPL), apolipoproteins such as apolipoprotein C-III (ApoC-III), and angiopoietin-like proteins (ANGPTLs). Targeting these proteins in the metabolic cascade has shown promising results in reducing triglyceride levels. Emerging therapies such as antisense oligonucleotides (ASOs) and small interfering RNA (siRNA) directed against ApoC-III (volanesorsen, olezarsen, and plozasiran), inhibitors of ANGPTL3 (evinacumab and zodasiran), and fibroblast growth factor 21 (FGF-21) analogs (pegozafermin) have demonstrated substantial triglyceride-lowering efficacy. These agents have achieved reductions in triglyceride levels of up to 80% in clinical trials. Additionally, preliminary evidence suggests that these agents may also reduce the incidence of acute pancreatitis and improve cardiometabolic risk profiles, although dedicated trials are still needed to confirm these outcomes. The therapeutic landscape for hypertriglyceridemia is rapidly evolving. Integrating these novel agents into clinical practice will require individualized treatment plans, sustained lifestyle modification, and careful safety monitoring. Full article
(This article belongs to the Special Issue Metabolic Alterations in Health and Disease: From Molecular Mechanisms to Biomarkers in Clinical Applications)
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21 pages, 1373 KB  
Review
Oxidative Stress, Mitochondrial Homeostasis, and Sirtuins in Atrial Fibrillation
by Jan Krekora, Elzbieta Pawlowska, Marcin Derwich, Jarosław Drożdż and Janusz Blasiak
Int. J. Mol. Sci. 2026, 27(1), 175; https://doi.org/10.3390/ijms27010175 - 23 Dec 2025
Cited by 6 | Viewed by 2230
Abstract
Atrial fibrillation (AF) is the most common cardiac arrhythmia. Yet, its treatment has serious challenges and is unsuccessful in a considerable fraction of patients. One reason may be a limited understanding of the molecular mechanisms underlying AF. Recent studies suggest that oxidative stress [...] Read more.
Atrial fibrillation (AF) is the most common cardiac arrhythmia. Yet, its treatment has serious challenges and is unsuccessful in a considerable fraction of patients. One reason may be a limited understanding of the molecular mechanisms underlying AF. Recent studies suggest that oxidative stress is involved in AF pathogenesis. Enhanced oxidative stress is largely determined by disrupted mitochondrial homeostasis, as cardiomyocytes heavily rely on mitochondrial energy production and calcium transfer between mitochondria and the sarcoplasmic reticulum. Atrial fibrillation involves metabolic, structural, and electrical remodeling, all of which are influenced by mitochondrial mechanisms. Mitochondrial homeostasis is controlled by mitochondrial quality control (mtQC), which is a multi-pathway mechanism to maintain integrity and functionality of mitochondria. Impaired mtQC may result in disturbed mitochondria-related calcium handling, decreased energy production, mitochondria-related inflammation and fibrosis, and impaired mitophagy. Sirtuins (SIRTs) are a family of seven members of histone deacetylases which have antioxidant properties, and three of them are localized to mitochondria. Therefore, at least some SIRTs may ameliorate enhanced oxidative stress related to damaged mitochondria. SIRTs have shown potential to improve AF outcomes in studies on AF patients and animal models. Therefore, SIRTs may have potential to ameliorate AF by decreasing oxidative stress and restoring mitochondrial homeostasis disrupted in AF. In this narrative review, we provide information on how mitochondrial dysfunctions, expressed as a disturbance in mtQC, contribute to AF through oxidative stress, calcium handling abnormalities, energy deficiency, inflammation and fibrosis, and genetic changes. In addition, we present the protective potential of sirtuins in AF. Full article
(This article belongs to the Special Issue Metabolic Alterations in Health and Disease: From Molecular Mechanisms to Biomarkers in Clinical Applications)
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