Evidence map›Paper›PMID 41128021›Full record

ReviewBiomolecules & biomedicine2025

Mitochondrial dysfunction, reactive oxygen species, and diabetes mellitus - A triangular relationship: A review.

Mia Manojlovic, Sonja Zafirovic, Dragana Tomic Naglic, Edita Stokic, Manfredi Rizzo, Jasjit S Suri, Esma Isenovic

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Biomolecules & biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Mia ManojlovicUniversity of Novi Sad, Faculty of Medicine in Novi Sad, Novi Sad, Serbia; Clinic for Endocrinology, Diabetes and Metabolic Disorders, University Clinical Center of Vojvodina, Novi Sad, Serbia.
Sonja ZafirovicDepartment of Radiobiology and Molecular Genetics, "VINČA" Institute of Nuclear Sciences - National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Dragana Tomic NaglicUniversity of Novi Sad, Faculty of Medicine in Novi Sad, Novi Sad, Serbia; Clinic for Endocrinology, Diabetes and Metabolic Disorders, University Clinical Center of Vojvodina, Novi Sad, Serbia.
Edita StokicUniversity of Novi Sad, Faculty of Medicine in Novi Sad, Novi Sad, Serbia; Clinic for Endocrinology, Diabetes and Metabolic Disorders, University Clinical Center of Vojvodina, Novi Sad, Serbia.
Manfredi RizzoSchool of Medicine, Promise Department, University of Palermo, Italy; Ras Al Khaimah Medical and Health Sciences University, Ras Al Khaimah, United Arab Emirates.
Jasjit S SuriStroke Diagnostic and Monitoring Division, AtheroPoint, Roseville, CA, USA; Department of Electrical and Computer Engineering, Idaho State University, Pocatello, ID, USA; Global Biomedical Technologies, Inc., Roseville, CA, USA; Symbiosis Institute of Technology, Nagpur Campus, Symbiosis International (Deemed University), Pune, India.
Esma IsenovicDepartment of Radiobiology and Molecular Genetics, "VINČA" Institute of Nuclear Sciences - National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus (DM) disrupts cellular homeostasis and is characterized by mitochondrial structural and functional impairments similar to those found in other metabolic disorders. Mitochondrial dysfunction (MD) leads to the excessive production of reactive oxygen species (ROS), which are central to the progression of cardiovascular (CV) disease-the leading cause of mortality associated with DM. ROS-driven oxidative stress (OS) is implicated in cardiac injury in both clinical and experimental contexts. This review synthesizes recent literature on the role of MD in the development and progression of DM and its associated CV complications, highlighting disrupted pathways that regulate the balance between ROS production and antioxidant defenses. We summarize alterations in mitochondrial dynamics-including fusion, fission, and mitophagy-mtDNA damage, and impaired oxidative phosphorylation characterized by dysregulated mitochondrial membrane potential (ΔΨm), electron transport chain (ETC) defects, uncoupling, and substrate overload. Additionally, we discuss hyperglycemia-activated pathways such as polyol flux, AGE-RAGE interactions, protein kinase C/nicotinamide adenine dinucleotide phosphate (PKC/NADPH) oxidase activation, and poly(ADP-ribose) polymerase 1 (PARP-1)-mediated glyceraldehyde-3-phosphate dehydrogenase (GAPDH) inhibition, which contribute to inflammation, endothelial dysfunction, β-cell failure, insulin resistance, and micro/macrovascular injury. Diagnostic and biomarker strategies encompass mtDNA analysis, bioenergetic assays, metabolomics, proteomics, and imaging techniques including PET, MRI, and NIRS. Therapeutic approaches aimed at restoring mitochondrial function and mitigating OS include mitochondria-targeted antioxidants (such as MitoQ, CoQ10, SkQ1, SS-31, and Mito-TEMPO), metabolic drugs (including metformin and SGLT2 inhibitors), lifestyle modifications, and emerging gene-editing technologies. The interplay between mitochondria, ROS, and DM reflects a tightly regulated aspect of cellular physiology; while targeted and personalized strategies hold promise, they necessitate rigorous evaluation.

Indexed as

Diabetes MellitusMitochondriaReactive Oxygen SpeciesAnimalsHumansOxidative StressReactive Oxygen Species

Identifiers

PMID41128021
PMCPMC12710611

What Socratic holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.