ArticleStem cell research & therapy2024
Single-cell sequencing of facial adipose tissue unveils FKBP5 as a therapeutic target for facial infiltrating lipomatosis.
Article in Stem cell research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- SPSB1 Promotes Subcutaneous Adipose Hyperplasia in Facial Port-Wine Stains by Controlling HDAC1 Degradation and Stability Through Two Distinct Proteolytic Pathways.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PIK3CA Mutations Downregulate PPT1 to Promote Adipogenesis by Suppressing P300 Depalmitoylation and Phase Separation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The mechanism and clinical significance of FKBP5 gene DNA methylation in various psychiatric, metabolic and tumor-related diseases.Frontiers in genetics · 2026Review
- Inhibition of FKBP5 alleviates obstetric antiphospholipid syndrome by regulating macrophage polarization.Scientific reports · 2025Article
- FKBP5 Regulates Osteogenesis of Human iPSC-Derived Mesenchymal Stem Cells via FKBP5-AKT-FOXO1 Pathway.Journal of cellular and molecular medicine · 2025Article
- H3K18 lactylation-hexokinase 2 positive feedback loop promotes osteogenesis of ASPCs in facial infiltrating lipomatosis.Stem cell research & therapy · 2025Article
- Extramedullary relapse of acute lymphoblastic leukemia treated with a CAR-T cell therapy bridge to unrelated cord blood transplantation: a case report and review of the literature.Frontiers in oncology · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundFacial infiltrating lipomatosis is characterized by excessive growth of adipose tissue. Its etiology is associated with somatic phosphatidylinositol 3-kinase catalytic subunit alpha (PIK3CA) variants, but the specific mechanisms are not yet fully understood.
methodsWe collected facial adipose tissue from both FIL patients and non-FIL individuals, isolated the stromal vascular fraction (SVF) and performed single-cell transcriptome sequencing on these samples.
resultsWe mapped out the cellular landscape within the SVF, with a specific focus on a deeper analysis of fibro-adipogenic precursor cells (FAPs). Our analysis revealed that FAPs from FIL patients (FIL-FAPs) significantly overexpressed FK506 binding protein 51 (FKBP5) compared to FAPs from individuals without FIL. Further experiments indicated that FKBP5 is regulated by the PI3K-AKT signaling pathway. The overactivation of this pathway led to an increase in FKBP5 expression. In vitro experiments demonstrated that FKBP5 promoted adipogenic differentiation of FAPs, a process that could be hindered by FKBP5 knockdown or inhibition. Additionally, in vivo assessments confirmed FKBP5's role in adipogenesis.
conclusionsThese insights into the pathogenesis of FIL underscore FKBP5 as a promising target for developing non-surgical interventions to manage the excessive adipose tissue growth in FIL.
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