BACKGROUND: Striae gravidarum (SG) is a common skin condition characterized by disrupted dermal extracellular matrix (ECM) homeostasis. Despite its high prevalence, the underlying cellular and molecular pathogenesis remains poorly understood, particularly regarding fibroblast heterogeneity and metabolic dysregulation. OBJECTIVES: This study aimed to delineate the cellular landscape and molecular mechanisms of SG at single-cell resolution, with a focus on fibroblast subpopulation dynamics, intercellular communication, and metabolic reprogramming. METHODS: We performed integrated single-cell RNA sequencing (scRNA-seq) and single-nucleus RNA sequencing (snRNA-seq) on dermal specimens from human SG lesions and matched normal skin. Functional validation was conducted using qPCR, histological staining (H notably, it also downregulated representative sC7-associated genes while upregulating sC5-associated genes, suggesting partial restoration of a reparative transcriptional program. Furthermore, local Acsbg1 silencing in dorsal skin alleviated SG-like dermal remodeling in the mouse model, with improved dermal architecture, collagen organization, and elastic fiber integrity. CONCLUSIONS: Targeting ACSBG1-mediated fatty acid metabolic reprogramming in pro-fibrotic fibroblast subsets restores a reparative transcriptional programme and ameliorates dermal ECM disruption in SG. These findings identify ACSBG1 as a potential therapeutic target for SG.
Cheng et al. (2026) studied this question.