ArticleScientific reports2017
Energetic mitochondrial failing in vitiligo and possible rescue by cardiolipin.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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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.
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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.
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Who cites it
37 citing papers in PubMed, 61 citations in OpenAlex.
- Markers of Systemic Metabolic Dysfunction in Vitiligo and Their Potential Role in Disease Pathogenesis: A Narrative Review.Health science reports · 2026Article
- Review
- Vitiligo.Nature reviews. Disease primers · 2025Review
- Dysregulated Intracellular Signaling in the Pathogenesis of Vitiligo: An Update on Emerging Therapeutic Strategies.Biomedicines · 2025Review
- Article
- Mitochondria in cutaneous health, disease, ageing and rejuvenation-the 3PM-guided mitochondria-centric dermatology.The EPMA journal · 2025Article
- Metabolic anomalies in vitiligo: a new frontier for drug repurposing strategies.Frontiers in pharmacology · 2025Article
- Markers of Metabolic Abnormalities in Vitiligo Patients.International journal of molecular sciences · 2024Article
- Review
- Dermatologic Manifestations of Mitochondrial Dysfunction: A Review of the Literature.International journal of molecular sciences · 2024Review
- An Overview of the Biological Complexity of Vitiligo.Oxidative medicine and cellular longevity · 2024Review
- The Role of Oxidative Stress in Vitiligo: An Update on Its Pathogenesis and Therapeutic Implications.Cells · 2023Review
- Melanin: a unifying theory of disease as exemplified by Parkinson's, Alzheimer's, and Lewy body dementia.Frontiers in immunology · 2023Article
- Antioxidant mechanisms of mesenchymal stem cells and their therapeutic potential in vitiligo.Frontiers in cell and developmental biology · 2023Review
- Damage-associated molecular patterns in vitiligo: igniter fuse from oxidative stress to melanocyte loss.Redox report : communications in free radical research · 2022Review
- Article
- Regenerative Medicine-Based Treatment for Vitiligo: An Overview.Biomedicines · 2022Review
- Altered epidermal proliferation, differentiation, and lipid composition: Novel key elements in the vitiligo puzzle.Science advances · 2022Article
- Focus on the Contribution of Oxidative Stress in Skin Aging.Antioxidants (Basel, Switzerland) · 2022Review
- Role of HMGB1 in Vitiligo: Current Perceptions and Future Perspectives.Clinical, cosmetic and investigational dermatology · 2022Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vitiligo is characterized by death or functional defects of epidermal melanocytes through still controversial pathogenic process. Previously, we showed that mitochondria-driven pre-senescent phenotype diminishes the capability of vitiligo melanocytes to cope with stressful stimuli. In the current study, we investigated markers of mitochondrial energy metabolism including the PGC1a axis, and then we determined the index of mitochondrial impairment using a cytomic approach. We found in cultured epidermal vitiligo melanocytes, compared to healthy ones, low ATP, increased proton leakage, and altered expression of several glycolytic enzymes (hexokinase II, pyruvic dehydrogenase kinase 1 and pyruvic kinase M2), We suggest that the low ATP production may be sufficient in steady-state conditions but it is unable to cover further needs. We also found in vitiligo melanocyrtes hyper-activation of the PGC1α axis, finalized to counteract the energy defect. Cytomic analysis, supported by MitoTracker Red pattern and ex-vivo immunohistochemistry, suggested an increased mitochondrial mass, possibly useful to ensure the essential ATP level. Finally, pharmacological cardiolipin stabilization reverted the energetic impairment, confirming the initial mitochondrial role. In conclusion, we report new insight in the pathogenetic mechanism of viitligo and indicate that the mitochondrial failure rescue by cardiolipin manipulation may be a new intriguing target in treatment development.
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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 OpenQuestion graph.