Trial reportThe Journal of biological chemistry2013
Mechanisms of mitochondrial damage in keratinocytes by pemphigus vulgaris antibodies.
Trial report in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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.
Who cites it
23 citing papers in PubMed, 56 citations in OpenAlex.
- Targeting ST18-mediated pathomechanism in pemphigus vulgaris through voltage-dependent anion channel inhibition.Skin health and disease · 2026Article
- Desmoglein-driven dynamic signaling in pemphigus vulgaris: a systematic review of pathogenic pathways.NPJ Regenerative medicine · 2025Article
- Novel Serum Oxidative Stress Biomarkers in Pemphigus Vulgaris: Clinical Insights and Implications for Pathogenesis.Dermatology practical & conceptual · 2025Article
- Ocular Mucous Membrane Pemphigoid Demonstrates a Distinct Autoantibody Profile from Those of Other Autoimmune Blistering Diseases: A Preliminary Study.Antibodies (Basel, Switzerland) · 2024Article
- Navigating neurological disorders: harnessing the power of natural compounds for innovative therapeutic breakthroughs.EXCLI journal · 2024Review
- The Role of Non-Neuronal Acetylcholine in the Autoimmune Blistering Disease Pemphigus Vulgaris.Biology · 2023Review
- Multifaceted roles of mitochondria in wound healing and chronic wound pathogenesis.Frontiers in cell and developmental biology · 2023Review
- Mitochondrial Autoantibodies and the Role of Apoptosis in Pemphigus Vulgaris.Antibodies (Basel, Switzerland) · 2022Review
- Apoptolysis: a less understood concept in the pathogenesis of Pemphigus Vulgaris.Apoptosis : an international journal on programmed cell death · 2022Review
- Marked to Die-Cell Death Mechanisms for Keratinocyte Acantholysis in Pemphigus Diseases.Life (Basel, Switzerland) · 2022Review
- Electron microscopy of desmosomal structures in the pemphigus human skin organ culture model.Frontiers in medicine · 2022Article
- The Immunogenetics of Autoimmune Blistering Diseases.Advances in experimental medicine and biology · 2022Review
- IgG4 Autoantibodies in Organ-Specific Autoimmunopathies: Reviewing Class Switching, Antibody-Producing Cells, and Specific Immunotherapies.Frontiers in immunology · 2022Review
- Mechanisms of Trx2/ASK1-Mediated Mitochondrial Injury in Pemphigus Vulgaris.BioMed research international · 2021Article
- Mitochondria in skin health, aging, and disease.Cell death & disease · 2020Review
- Immunoadsorption of Desmoglein-3-Specific IgG Abolishes the Blister-Inducing Capacity of Pemphigus Vulgaris IgG in Neonatal Mice.Frontiers in immunology · 2018Article
- The Evolving Story of Autoantibodies in Pemphigus Vulgaris: Development of the "Super Compensation Hypothesis".Frontiers in medicine · 2018Review
- Autoantibody Signaling in Pemphigus Vulgaris: Development of an Integrated Model.Frontiers in immunology · 2018Review
- Loss of Desmoglein Binding Is Not Sufficient for Keratinocyte Dissociation in Pemphigus.The Journal of investigative dermatology · 2015Article
- Critical Role of the Neonatal Fc Receptor (FcRn) in the Pathogenic Action of Antimitochondrial Autoantibodies Synergizing with Anti-desmoglein Autoantibodies in Pemphigus Vulgaris.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The development of nonhormonal treatment of pemphigus vulgaris (PV) has been hampered by a lack of clear understanding of the mechanisms leading to keratinocyte (KC) detachment and death in pemphigus. In this study, we sought to identify changes in the vital mitochondrial functions in KCs treated with the sera from PV patients and healthy donors. PV sera significantly increased proton leakage from KCs, suggesting that PV IgGs increase production of reactive oxygen species. Indeed, measurement of intracellular reactive oxygen species production showed a drastic increase of cell staining in response to treatment by PV sera, which was confirmed by FACS analysis. Exposure of KCs to PV sera also caused dramatic changes in the mitochondrial membrane potential detected with the JC-1 dye. These changes can trigger the mitochondria-mediated intrinsic apoptosis. Although sera from different PV patients elicited unique patterns of mitochondrial damage, the mitochondria-protecting drugs nicotinamide (also called niacinamide), minocycline, and cyclosporine A exhibited a uniform protective effect. Their therapeutic activity was validated in the passive transfer model of PV in neonatal BALB/c mice. The highest efficacy of mitochondrial protection of the combination of these drugs found in mitochondrial assay was consistent with the ability of the same drug combination to abolish acantholysis in mouse skin. These findings provide a theoretical background for clinical reports of the efficacy of mitochondria-protecting drugs in PV patients. Pharmacological protection of mitochondria and/or compensation of an altered mitochondrial function may therefore become a novel approach to development of personalized nonhormonal therapies of patients with this potentially lethal autoimmune blistering disease.
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Registered trials
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.