ArticlePloS one2012
Sterol intermediates of cholesterol biosynthesis inhibit hair growth and trigger an innate immune response in cicatricial alopecia.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Cross-species comparative spatial transcriptomics of hair follicle-T cell interactions identifies conserved drivers of cutaneous lupus erythematosus skin disease and associated hair loss.Nature communications · 2026Article
- Cholesterol promotes hair growth through activating sympathetic nerves and enhancing the proliferation of hair follicle stem cells.Molecular medicine (Cambridge, Mass.) · 2025Article
- Frontal Fibrosing Alopecia: An Update.American journal of clinical dermatology · 2025Review
- Disrupted cholesterol biosynthesis and hair follicle stem cell impairment in the onset of alopecia.PloS one · 2025Article
- Proteomic Profiling of Central Centrifugal Cicatricial Alopecia Reveals Role of Humoral Immune Response Pathway and Metabolic Dysregulation.JID innovations : skin science from molecules to population health · 2024Article
- Analysis of Copy Number Variation in the Whole Genome of Normal-Haired and Long-Haired Tianzhu White Yaks.Genes · 2022Article
- Primary cicatricial alopecias are characterized by dysregulation of shared gene expression pathways.PNAS nexus · 2022Article
- Destruction of the stem cell Niche, Pathogenesis and Promising Treatment Targets for Primary Scarring Alopecias.Stem cell reviews and reports · 2020Review
- Biallelic pathogenic variants in the lanosterol synthase gene LSS involved in the cholesterol biosynthesis cause alopecia with intellectual disability, a rare recessive neuroectodermal syndrome.Genetics in medicine : official journal of the American College of Medical Genetics · 2019Article
- Accumulation of specific sterol precursors targets a MAP kinase cascade mediating cell-cell recognition and fusion.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Investigating the effects of metabolic dysregulation on hair follicles: a comparison of HIV-infected women with and without central lipohypertrophy.International journal of dermatology · 2014Article
- Beyond goosebumps: does the arrector pili muscle have a role in hair loss?International journal of trichology · 2014Review
- Mutations in the cholesterol transporter gene ABCA5 are associated with excessive hair overgrowth.PLoS genetics · 2014Article
- Arabidopsis ERG28 tethers the sterol C4-demethylation complex to prevent accumulation of a biosynthetic intermediate that interferes with polar auxin transport.The Plant cell · 2013Article
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Authors and funding
7 authors.
Funding
Abstract
Primary cicatricial alopecia (PCA) is a group of inflammatory hair disorders that cause scarring and permanent hair loss. Previous studies have implicated PPARγ, a transcription factor that integrates lipogenic and inflammatory signals, in the pathogenesis of PCA. However, it is unknown what triggers the inflammatory response in these disorders, whether the inflammation is a primary or secondary event in disease pathogenesis, and whether the inflammatory reaction reflects an autoimmune process. In this paper, we show that the cholesterol biosynthetic pathway is impaired in the skin and hair follicles of PCA patients. Treatment of hair follicle cells with BM15766, a cholesterol biosynthesis inhibitor, or 7-dehydrocholesterol (7-DHC), a sterol precursor, stimulates the expression of pro-inflammatory chemokine genes. Painting of mouse skin with 7-DHC or BM15766 inhibits hair growth, causes follicular plugging and induces the infiltration of inflammatory cells into the interfollicular dermis. Our results demonstrate that cholesterologenic changes within hair follicle cells trigger an innate immune response that is associated with the induction of toll-like receptor (TLR) and interferon (IFN) gene expression, and the recruitment of macrophages that surround the hair follicles and initiate their destruction. These findings reveal a previously unsuspected role for cholesterol precursors in PCA pathogenesis and identify a novel link between sterols and inflammation that may prove transformative in the diagnosis and treatment of these disorders.
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