Evidence map›Paper›PMID 20436882›Full record

ArticleDermato-endocrinology2009

Role of FGFR2-signaling in the pathogenesis of acne.

Bodo C Melnik

Open access · bronzeAbstract read
In one paragraph

Article in Dermato-endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.6field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. The Immunogenetics of Acne.Advances in experimental medicine and biology · 2022
    Article
  9. Acne Syndromes and Mosaicism.Biomedicines · 2021
    Review
  10. Review
  11. Acne and craniofacial defects.JAAD case reports · 2019
    Article
  12. Review
  13. Article
  14. Article
  15. Beyond acne: Current aspects of sebaceous gland biology and function.Reviews in endocrine & metabolic disorders · 2016
    Review
  16. Article
  17. Linking diet to acne metabolomics, inflammation, and comedogenesis: an update.Clinical, cosmetic and investigational dermatology · 2015
    Review
  18. Review
  19. The molecular and cellular basis of Apert syndrome.Intractable & rare diseases research · 2013
    Review
  20. [Uncommon acne-associated syndromes and their significance in understanding the pathogenesis of acne].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2013
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Bodo C MelnikDepartment of Dermatology; Environmental Medicine and Health Theory; University of Osnabrück; Germany.
Osnabrück University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is the purpose of this review to extend our understanding of the fibroblast growth factor (FGF) receptor-2b-signaling network in the pathogenesis of acne. A new concept of the role of FGFR2b-signaling in dermal-epithelial interaction for skin appendage formation, pilosebaceous follicle homeostasis, comedogenesis, sebaceous gland proliferation and lipogenesis is presented. The FGFR2-gain-of-function mutations in Apert syndrome and unilateral acneiform nevus are most helpful model diseases pointing the way to androgen-dependent dermalepithelial FGFR2-signaling in acne. Androgen-mediated upregulation of FGFR2b-signaling in acne-prone skin appears to be involved in the pathogenesis of acne vulgaris. In organotypic skin cultures, keratinocyte-derived interleukin-1alpha stimulated fibroblasts to secrete FGF7 which stimulated FGFR2b-mediated keratinocyte proliferation. Postnatal deletion of FGFR2b in mice resulted in severe sebaceous gland atrophy. The importance of FGFR2b in sebaceous gland physiology is further supported by the mode of action of anti-acne agents which have been proposed to attenuate FGFR2b-signaling. Downregulation of FGFR2b-signaling by isotretinoin explains its therapeutic effect in acne. Downregulation of FGFR2b-signaling during the first trimester of pregnancy disturbs branched morphogenesis and explains retinoid embryotoxicity. Insulin-like growth factor-1 (IGF-1), the mediator of growth hormone during puberty, intracts with androgen-dependent FGFR2b-signaling and links androgen- and FGF-mediated signal transduction important in sebaceous gland homeostasis. The search for a follicular defect in the dermalepithelial regulation of growth factor-signaling in acne-prone skin appears to be a most promising approach to clarify the pathogenesis of acne.

Indexed as

acneApert syndromecomedogenesisfibroblast growth factor receptor-2fibroblast growth factorsinsulininsulin-like growth factor-1interleukin-1αnevus comedonicussebogenesisunilateral acneiform nevus

Identifiers

PMID20436882
PMCPMC2835907
OpenAlexW1976176052

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.