Research progress on the role of melanocyte stem cell dysfunction in the pathogenesis of vitiligo
Xue Linnan
Cao Shi
Sun Hetong
Sang Chenchen
Fang Gaoge
Liang Yuying
Zhang Shidi
Wang Yuanhong
Abstract:Vitiligo is a common autoimmune dermatosis characterized by skin depigmentation.Recent studies indicate that the impairment and functional decline of melanocyte stem cells(McSCs)serve as a critical basis for persistent depigmenta-tion and limited repigmentation in vitiligo.Under the influence of genetic factors,oxidative stress,and the interferon-γ(IFN-γ)-driven C-X-C motif ligand 9(CXCL9)/C-X-C motif ligand 10(CXCL10)-C-X-C motif chemokine receptor 3(CXCR3)signaling axis,McSCs become more vulnerable to damage,with markedly reduced capacities for survival,differ-entiation,and migration,thereby hindering the re-establishment of a stable pigment cell reservoir.This review summarizes the primary molecular and cellular mechanisms underlying McSC damage.Furthermore,by integrating current treatment modalities such as phototherapy,topical immunomodulators,stem cell transplantation,and novel biologics,it discusses the roles and limitations of these interventions in improving McSC function.Recent research trends reveal a shift in vitiligo treatment from merely suppressing immune responses towards comprehensive strategies that regulate the immune microen-vironment and promote stem cell regeneration.However,further investigation is warranted into the regenerative patterns of McSCs,the remodeling of the local microenvironment,and the pathways to achieving personalized therapy.This review aims to provide references for subsequent basic research and clinical innovation focusing on McSCs.
Keywords:VitiligoMelanocyte stem cellsDysfunctionDamage mechanismImmune responseTreatment strategy
Publication Date:2025-12-20
Online Publishing Date:2026-03-09(First online date of this platform, not the publication date of the document)
Pages:6( 151-156 )
Health Medicine Research and Practice

Health Medicine Research and Practice

ISTIC
ISSN:1673-873X
Year, Vol.(Issue):2025,22(12)