{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE326nnn/GSE326094/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Other"],"species":["Homo sapiens"],"gds_type":["Other"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE326094"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Aberrant laminin signaling drives melanocyte dedifferentiation and unveils a tractable therapeutic target in vitiligo","description":"Vitiligo is characterized by progressive loss of melanocytes, but the underlying mechanisms governing melanocyte dysfunction remain incompletely understood. In this study, we aimed to investigate the role of the extracellular matrix microenvironment in regulating melanocyte identity and function. We performed spatial transcriptomics using the 10x Genomics Visium platform on human skin samples from healthy controls and vitiligo patients. This approach enabled spatially resolved analysis of gene expression changes associated with melanocyte dedifferentiation. Our analysis revealed that aberrant laminin signaling, particularly involving Laminin-332, is associated with transcriptional reprogramming of melanocytes toward a dedifferentiated state. Spatially resolved gene expression patterns indicated alterations in pathways related to cell adhesion, cytoskeletal organization, and stress responses in vitiligo lesions. These findings provide insight into how extracellular matrix remodeling contributes to melanocyte dysfunction and identify potential therapeutic targets for restoring melanocyte differentiation in vitiligo.","dates":{"publication":"2026/04/16"},"accession":"GSE326094","cross_references":{"GSM":["GSM9622152"],"GPL":["24676"],"GSE":["326094"],"taxon":["Homo sapiens"]}}