Redox Mechanisms in Obesity-Induced Organ Injury: Potential Therapeutic Opportunities
A Special Issue of Antioxidants (ISSN 2076-3921) belonging to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: 10 December 2026 | Viewed by 173
Editors
Interests: obesity; diabetes; insulin resistance; mitochondrial dysfunction; oxidative stress; liver; adipose tissue; liver-brain axis; endogenous lipid mediators; N-acylethanolamines; preclinical model
Special Issues, Collections and Topics in MDPI journals
Interests: obesity; insulin resistance; mitochondrial dysfunction; oxidative stress; liver metabolism; adipose tissue biology; liver–brain axis; lipid mediators; N-acylethanolamines; preclinical models
Special Issue Information
Dear Colleagues,
Obesity is a major global health challenge and a key driver of multiple chronic diseases, including metabolic, cardiovascular, and liver disorders. A growing body of evidence indicates that redox imbalance plays a central role in mediating obesity-induced organ injury, affecting a wide range of tissues such as the liver, adipose tissue, heart, and brain. Excess nutrient availability and metabolic overload promote the generation of reactive oxygen species (ROS), leading to oxidative stress, mitochondrial dysfunction, and activation of redox-sensitive signaling pathways.
These alterations contribute to tissue damage, inflammation, and progressive dysfunction, ultimately driving the development of conditions such as MAFLD/MASH, insulin resistance, cardiovascular disease, and neurodegeneration. In addition, redox-dependent mechanisms are increasingly recognized as critical modulators of inter-organ communication, further amplifying systemic metabolic disturbances.
This Special Issue aims to provide a comprehensive overview of the molecular and cellular mechanisms underlying redox-mediated organ injury in obesity, with a focus on mechanistic insights and therapeutic opportunities. We welcome original research articles and reviews addressing oxidative stress, mitochondrial dysfunction, extracellular vesicles, inflammatory signaling, and metabolic dysregulation, as well as studies exploring novel strategies targeting redox pathways to prevent or reverse obesity-associated complications.
Dr. Claudio Pirozzi
Guest Editor
Dr. Stefania Melini
Guest Editor Assistant
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. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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
- redox signaling
- oxidative stress
- metabolic diseases
- mitochondrial dysfunction
- inflammation
- liver
- brain
- MAFLD (metabolic dysfunction-associated fatty liver disease)
- MASH (metabolic dysfunction-associated steatohepatitis)
- cardiometabolic diseases
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