ArticleInflammation2025
Sirtuin1 Deficiency Could Exacerbate Melanocyte Apoptosis Under Endoplasmic Reticulum Stress.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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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Who cites it
2 citing papers in PubMed.
- Role of MAPK Pathways in the Pathogenesis of Vitiligo.Current issues in molecular biology · 2026Review
- Dysregulated Intracellular Signaling in the Pathogenesis of Vitiligo: An Update on Emerging Therapeutic Strategies.Biomedicines · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
Vitiligo is a depigmentation disease caused by the targeted destruction of melanocytes, resulting in skin and hair depigmentation and significant psychological stress. However, the mechanisms underlying its onset and progression remain unclear. Endoplasmic reticulum (ER) stress, which is linked with oxidative stress and autoimmunity, is involved in the development of vitiligo, and prolonged ER stress induces apoptosis. Sirtuin 1 (Sirt1) might be a key regulator of ER stress. Thus, we explored how Sirt1 modulates ER stress-induced melanocyte apoptosis in vitro and in vivo. Our results showed that Sirt1 affected ER stress-induced apoptosis of melanocyte apoptosis when upon to ER stress in vitro. Sirt1 inhibition aggravated the vitiligo phenotype in mice; thereby protecting against the stress response, and abating the unfolded protein response. These results suggest that Sirt1 impairment could accelerate melanocyte apoptosis in vitiligo.
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