ReviewAntibodies (Basel, Switzerland)2022
Mitochondrial Autoantibodies and the Role of Apoptosis in Pemphigus Vulgaris.
Review in Antibodies (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- IL‑37/IL‑1R8 blocks keratinocyte acantholysis via suppressing ADAM17/EGFR.International journal of molecular medicine · 2026Article
- Targeting ST18-mediated pathomechanism in pemphigus vulgaris through voltage-dependent anion channel inhibition.Skin health and disease · 2026Article
- Antimitochondrial antibodies in systemic sclerosis target enteric neurons and are associated with GI dysmotility.Annals of the rheumatic diseases · 2025Article
- Autoimmune pemphigus: difficulties in diagnosis and the molecular mechanisms underlying the disease.Frontiers in immunology · 2025Review
- An Overview of Clinical Manifestations of Dermatological Disorders in Intensive Care Units: What Should Intensivists Be Aware of?Diagnostics (Basel, Switzerland) · 2023Review
- 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
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pemphigus vulgaris (PV) is an IgG autoantibody-mediated, potentially fatal mucocutaneous disease manifested by progressive non-healing erosions and blisters. Beyond acting to inhibit adhesion molecules, PVIgGs elicit a unique process of programmed cell death and detachment of epidermal keratinocytes termed apoptolysis. Mitochondrial damage by antimitochondrial antibodies (AMA) has proven to be a critical link in this process. AMA act synergistically with other autoantibodies in the pathogenesis of PV. Importantly, absorption of AMA inhibits the ability of PVIgGs to induce blisters. Pharmacologic agents that protect mitochondrial function offer a new targeted approach to treating this severe immunoblistering 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.