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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). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 31 May 2026 | Viewed by 202

Special Issue 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-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

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

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Published Papers (1 paper)

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Review

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
Viewed by 102
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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