The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
Mechanisms of melanocyte death in vitiligo
Open accessAbstract
Vitiligo is an autoimmune depigment disease results from extensive melanocytes destruction. The destruction of melanocyte is thought to be of multifactorial causation. Genome‐wide associated studies have identified single‐nucleotide polymorphisms in a panel of susceptible loci as risk factors in melanocyte death. But vitiligo onset can't be solely attributed to a susceptive genetic background. Oxidative stress triggered by elevated levels of reactive oxygen species accounts for melanocytic molecular and organelle dysfunction, a minority of melanocyte demise, and melanocyte‐specific antigens exposure. Of note, the self‐responsive immune function directly contributes to the bulk of melanocyte deaths in vitiligo. The aberrantly heightened innate immunity, type‐1‐skewed T helper, and incompetent regulatory T cells tip the balance toward autoreaction and CD8+ cytotoxic T lymphocytes finally execute the killing of melanocytes, possibly alarmed by resident memory T cells. In addition to the well‐established apoptosis and necrosis, we discuss several death modalities like oxeiptosis, ferroptosis, and necroptosis that are probably employed in melanocyte destruction. This review focuses on the various mechanisms of melanocytic death in vitiligo pathogenesis to demonstrate a panorama of that. We hope to provide new insights into vitiligo pathogenesis and treatment strategies by the review.
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Cites
Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease
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Ferroptosis as a p53-mediated activity during tumour suppression
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Pyroptosis: Gasdermin-Mediated Programmed Necrotic Cell Death
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Granzyme A from cytotoxic lymphocytes cleaves GSDMB to trigger pyroptosis in target cells
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Cited by
Baicalein inhibits RLS3-induced ferroptosis in melanocytes
Yang, M., Li, X., Li, H., Zhang, X., Liu, X., & Song, Y. (2021) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2021.05.010 · Cited by 53
Metadata
- Authors
- Chen, J., Li, S., & Li, C.
- Venue
- Medicinal Research Reviews
- Publisher
- Wiley
- Published
- 2020-11-17
- Volume
- 41
- Issue
- 2
- Pages
- 1138-1166
- ISSN
- 0198-6325 (ISSN-L)
- 1098-1128
- OpenAlex
- W3100014595
- Cited by
- 307
- References
- 19
- FWCI
- 12.29
- Type
- journal article
- Language
- en
- Open access
- hybrid
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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