ArticleGenes & development2022
KLF5 governs sphingolipid metabolism and barrier function of the skin.
Article in Genes & development, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Intrinsic Dysregulation and Environmental Modifiers in Hidradenitis Suppurativa: Toward an Integrated Pathophysiologic Model.Journal of clinical medicine · 2026Review
- Hidradenitis suppurativa: epidemiology, diagnosis, molecular pathogenesis and therapy.Molecular biomedicine · 2026Review
- H3K9me3 controls epidermis morphogenesis by regulating RNA Pol II dynamics at developmental promoters and enhancers.Nature communications · 2026Article
- The Multifaceted Role of Keratinocytes in Hidradenitis Suppurativa Pathogenesis.Experimental dermatology · 2026Review
- Degeneration and adaptive evolution of digits in ratite birds.Molecular biology and evolution · 2026Article
- Distinct roles for SETα and SETβ in early cell fate decisions.Nucleic acids research · 2026Article
- Dynamic epigenetic and transcriptomic reprogramming during embryonic skin development in goose (Anser anser domesticus).Functional & integrative genomics · 2026Article
- On-demand sIPN microneedles promote infected burn wound healing via microenvironment remodeling and activation of the Wnt-KLF5 regenerative axis.Theranostics · 2026Article
- Hidradenitis Suppurativa Tunnels: Unveiling a Unique Disease Entity.JID innovations : skin science from molecules to population health · 2025Review
- Single-cell chromatin landscapes associated with the burnt skin healing process in rats.Scientific data · 2025Article
- Stem cell activity-coupled suppression of endogenous retrovirus governs adult tissue regeneration.Cell · 2024Article
- Unbiased screening identifies regulators of cell-cell adhesion and treatment options in pemphigus.Nature communications · 2024Article
- Glucocorticoid receptor controls atopic dermatitis inflammation via functional interactions with P63 and autocrine signaling in epidermal keratinocytes.Cell death & disease · 2024Article
- Article
- The direct binding of bioactive peptide Andersonin-W1 to TLR4 expedites the healing of diabetic skin wounds.Cellular & molecular biology letters · 2024Article
- Article
- Integrated multi-omics analyses identify anti-viral host factors and pathways controlling SARS-CoV-2 infection.Nature communications · 2024Article
Corrections and comments
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Authors and funding
26 authors at 2 institutions in 1 country.
Funding
Abstract
Stem cells are fundamental units of tissue remodeling whose functions are dictated by lineage-specific transcription factors. Home to epidermal stem cells and their upward-stratifying progenies, skin relies on its secretory functions to form the outermost protective barrier, of which a transcriptional orchestrator has been elusive. KLF5 is a Krüppel-like transcription factor broadly involved in development and regeneration whose lineage specificity, if any, remains unclear. Here we report KLF5 specifically marks the epidermis, and its deletion leads to skin barrier dysfunction in vivo. Lipid envelopes and secretory lamellar bodies are defective in KLF5-deficient skin, accompanied by preferential loss of complex sphingolipids. KLF5 binds to and transcriptionally regulates genes encoding rate-limiting sphingolipid metabolism enzymes. Remarkably, skin barrier defects elicited by KLF5 ablation can be rescued by dietary interventions. Finally, we found that KLF5 is widely suppressed in human diseases with disrupted epidermal secretion, and its regulation of sphingolipid metabolism is conserved in human skin. Altogether, we established KLF5 as a disease-relevant transcription factor governing sphingolipid metabolism and barrier function in the skin, likely representing a long-sought secretory lineage-defining factor across tissue types.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.