Fibroblast growth factors, their receptors and signaling

Powers, C J; McLeskey, S W; Wellstein, A

doi:10.1677/erc.0.0070165

Cited by 1,332Fibroblast Growth Factor ResearchConnective Tissue Growth Factor ResearchAngiogenesis and VEGF in Cancer

Fibroblast growth factors, their receptors and signaling

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Powers, C J, McLeskey, S W, Wellstein, A·2000·Endocrine-related cancer

DOI 10.1677/erc.0.0070165

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Abstract

Fibroblast growth factors (FGFs) are small polypeptide growth factors, all of whom share in common certain structural characteristics, and most of whom bind heparin avidly. Many FGFs contain signal peptides for secretion and are secreted into the extracellular environment, where they can bind to the heparan-like glycosaminoglycans (HLGAGs) of the extracellular matrix (ECM). From this reservoir, FGFs may act directly on target cells, or they can be released through digestion of the ECM or the activity of a carrier protein, a secreted FGF binding protein. FGFs bind specific receptor tyrosine kinases in the context of HLGAGs and this binding induces receptor dimerization and activation, ultimately resulting in the activation of various signal transduction cascades. Some FGFs are potent angiogenic factors and most play important roles in embryonic development and wound healing. FGF signaling also appears to play a role in tumor growth and angiogenesis, and autocrine FGF signaling may be particularly important in the progression of steroid hormone-dependent cancers to a hormone-independent state.

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GHK-Cu increases the expression of bFGF and VEGF in irradiated human dermal fibroblasts at a concentration of 1 nM.
“GHK-Cu at a concentration of 1nM increases the expression of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) in irradiated human dermal fibroblasts, both of which aid blood vessel formation and blood flow into damaged tissues [4–6].”
From The potential of GHK as an anti-aging peptide (2020) · cites this paper as [5]
The sections on FGF signaling and repair discuss angiogenesis and wound healing, but do not address GHK-Cu treatment. Searches for GHK-Cu, irradiated dermal fibroblasts, and the 1 nM concentration found no passage reporting the claimed increase in bFGF or VEGF expression. (LLM, conf=0.76)
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Authors: Powers, C. J., McLeskey, S. W., & Wellstein, A.
Affiliations: Georgetown University (US)
ORCID: Wellstein, A
Venue: Endocrine-related cancer
Publisher: Bioscientifica
Published: 2000-09-01
Volume: 7
Issue: 3
Pages: 165-197
ISSN: 1351-0088 (ISSN-L)
1479-6821
DOI: 10.1677/erc.0.0070165
OpenAlex: W2138178479
Cited by: 1,332
References: 300
Citations by year: 2026: 10 · 2025: 17 · 2024: 26 · 2023: 22 · 2022: 34 · 2021: 48 · 2020: 45 · 2019: 37 · 2018: 26 · 2017: 49 · 2016: 65 · 2015: 61 · 2014: 50 · 2013: 66 · 2012: 58
FWCI: 3.02
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Endocrine Related Cancer (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
Keywords: fibroblast growth factor, fibroblast growth factor receptor, receptor tyrosine kinase, extracellular matrix, receptor dimerization, signal transduction, angiogenesis, embryonic development, wound healing, tumor growth, autocrine signaling, hormone-independent breast cancer
MeSH terms: Animals, Extracellular Matrix, Fibroblast Growth Factors, Glycosaminoglycans, Growth Substances, Humans, Neoplasms, Signal Transduction, Receptors, Fibroblast Growth Factor

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Fibroblast growth factors, their receptors and signaling

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