Fgf10: a paracrine-signaling molecule in development, disease, and regenerative medicine.
Itoh N., Ohta H.
Narrative Review on Systemic / IV, published in Curr Mol Med (2014) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Curr Mol Med (2014)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 24730525
- DOI
- 10.2174/1566524014666140414204829
Abstract (original English)
The Fgf family comprises 22 members with diverse functions in development, repair, metabolism, and neuronal activities. Fgf10 mediates biological responses by activating Fgf receptor 2b (Fgfr2b) with heparin/heparan sulfate in a paracrine manner. Fgf10 and Fgfr2b are expressed in mesenchymal and epithelial tissues, respectively. Fgf10 is an epithelial-mesenchymal signaling molecule. Fgf10 knockout mice show severe phenotypes with complete truncation of the fore- and hindlimbs and die shortly after birth due to impaired lung development, indicating that Fgf10 serves as an essential regulator of lung and limb formation. Fgf10 also has roles in the development of white adipose tissue, heart, liver, brain, kidney, cecum, ocular glands, thymus, inner ear, tongue, trachea, eye, stomach, prostate, salivary gland, mammary gland, and whiskers. The diverse phenotypes of Fgf10 knockout mice are closely related to those of Fgfr2 knockout mice, suggesting that Fgf10 acts as a major ligand for Fgfr2b in mouse multi-organ development. Aplasia of lacrimal and salivary glands and lacrimo-auriculo-dento-digital syndrome are caused by Fgf10 mutations in humans. Variants in Fgf10 may be involved in an increased risk for limb deficiencies and cleft lip and palate. Patients with Fgf10 haploinsufficiency have lung function parameters indicating chronic obstructive pulmonary disease. Fgf10 induces mig
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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