Downregulation of Lonp1 Promotes Melanocyte Pyroptosis via Suppressing Mitophagy and Activating NLRP3 Pathway in Vitiligo under Oxidative Stress.

Authors

Xin Huang, Tianqi Wei, Youming Guo, Jing Zhu, Lingling Luo, Zhaokang Zhou, Baiyi Zuo, Guanying Liu, Beilei Xu, Chengrang Li

Published in

Inflammation. Jun 17, 2026. Epub Jun 17, 2026.

Abstract

Vitiligo is an autoimmune skin disease characterized by the loss of epidermal melanocytes. Oxidative stress serves as a key initiating factor in its pathogenesis. Mitochondria, known as the powerhouse of the cell, perform multiple essential functions in eukaryotic cells and participate in melanocyte physiological processes. Lonp1 is a crucial mitochondrial matrix soluble protease involved in maintaining mtDNA stability, clearing aberrant proteins, and regulating mitochondrial homeostasis. Meanwhile, mitophagy serves as a crucial function within the mitochondrial quality control system, responsible for eliminating damaged mitochondria. Pyroptosis is a form of programmed cell death mediated by inflammasomes, accompanied by cell membrane pore formation and the release of inflammatory cytokines. This study confirmed that oxidative stress was associated with decreased Lonp1 in PIG1 cells, the human melanocyte line. This downregulation impairs mitochondrial homeostasis by suppressing the expression of PINK1, a key mitophagy-related protein, ultimately leading to activation of the NLRP3 inflammasome pathway, release of IL-1β, and induction of melanocyte pyroptosis.

PMID:
42310240
Bibliographic data and abstract were imported from PubMed on 18 Jun 2026.

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