scholarly journals Fibroblast Growth Factor (FGF): A Review

2013 ◽  
Vol 01 (02) ◽  
pp. 091-094
Author(s):  
Ram Gupta ◽  
Manu Gupta ◽  
Avnika Garg
Keyword(s):  
Wound Healing ◽  
Growth Factors ◽  
Periodontal Regeneration ◽  
Fibroblast Growth Factors ◽  
Root Surface ◽  
Matrix Proteins ◽  
Fibroblast Growth ◽  
Polypeptide Growth Factors ◽  
Naturally Occurring ◽  
Periodontal Wound Healing

AbstractIn order for periodontal regeneration to occur, progenitor cells must migrate to the denuded root surface, attach to it, proliferate and mature into an organized and functional fibrous attachment apparatus. Significant advances have been made during the last decade in understanding the factors controlling the migration, attachment and proliferation of cells. A group of naturally occurring molecules known as polypeptide growth factors in conjunction with certain matrix proteins, are key regulators of these biological events. Of these, the fibroblast growth factors (FGFs) appear to have an important role in periodontal wound healing. The purpose of this review is to summarize current information on these growth factors with emphasis on their potential implications in periodontal wound healing and regeneration.

scholarly journals Regulation of Hepatic Stellate Cells and Fibrogenesis by Fibroblast Growth Factors

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Justin D. Schumacher ◽  
Grace L. Guo
Keyword(s):  
Wound Healing ◽  
Growth Factors ◽  
Hepatic Stellate Cells ◽  
Therapeutic Strategy ◽  
Fibroblast Growth Factors ◽  
Stellate Cells ◽  
Fibroblast Growth ◽  
Fgf Signaling ◽  
Paracrine Regulation ◽  
Hepatocyte Regeneration

Fibroblast growth factors (FGFs) are a family of growth factors critically involved in developmental, physiological, and pathological processes, including embryogenesis, angiogenesis, wound healing, and endocrine functions. In the liver, several FGFs are produced basally by hepatocytes and hepatic stellate cells (HSCs). Upon insult to the liver, expression of FGFs in HSCs is greatly upregulated, stimulating hepatocyte regeneration and growth. Various FGF isoforms have also been shown to directly induce HSC proliferation and activation thereby enabling autocrine and paracrine regulation of HSC function. Regulation of HSCs by the endocrine FGFs, namely, FGF15/19 and FGF21, has also recently been identified. With the ability to modulate HSC proliferation and transdifferentiation, targeting FGF signaling pathways constitutes a promising new therapeutic strategy to treat hepatic fibrosis.

scholarly journals Fibroblast growth factors, their receptors and signaling.

2000 ◽  
pp. 165-197 ◽  
Author(s):  
C J Powers ◽  
S W McLeskey ◽  
A Wellstein
Keyword(s):  
Growth Factors ◽  
Tyrosine Kinases ◽  
Structural Characteristics ◽  
Protein A ◽  
Fibroblast Growth Factors ◽  
Target Cells ◽  
Fibroblast Growth ◽  
Fgf Signaling ◽  
Independent State ◽  
Polypeptide Growth Factors

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.

scholarly journals Expression of fibroblast growth factors and their receptors during full-thickness skin wound healing in young and aged mice

2005 ◽  
Vol 186 (2) ◽  
pp. 273-289 ◽  
Author(s):  
Akiko Komi-Kuramochi ◽  
Mitsuko Kawano ◽  
Yuko Oda ◽  
Masahiro Asada ◽  
Masashi Suzuki ◽  
...  
Keyword(s):  
Wound Healing ◽  
Growth Factors ◽  
Growth Factor ◽  
Fibroblast Growth Factors ◽  
Fibroblast Growth ◽  
Full Thickness ◽  
Healthy Skin ◽  
Aged Mice ◽  
Full Thickness Skin ◽  
Thickness Skin

The highly ordered process of wound healing involves the coordinated regulation of cell proliferation and migration and tissue remodeling, predominantly by polypeptide growth factors. Consequently, the slowing of wound healing that occurs in the aged may be related to changes in the activity of these various regulatory factors. To gain additional insight into these issues, we quantified the absolute copy numbers of mRNAs encoding all the fibroblast growth factors (FGFs), their receptors (FGFRs) and two other growth factors in the dorsal skin of young and aged mice during the healing of full-thickness skin excisional wounds. In young adult mice (8 weeks old), FGF7, FGF10 and FGF22 mRNAs were all strongly expressed in healthy skin, and levels of FGF7 and 10 but not 22 increased 2- to 3.5-fold over differing time courses after wounding. The levels of FGF9, 16, 18 and especially 23 mRNAs were moderate or low in healthy skin but increased 2- to 33-fold after wounding. Among the four FGFRs, expression of only FGFR1 mRNA was augmented during wound healing. Expression of transforming growth factor-β and hepatocyte growth factor was also high in healthy skin and was upregulated during healing. Notably, in aged mice (35 weeks old), where healing proceeded more slowly than in the young, both the basal and wound-induced mRNA expression of most of these genes was reduced. While these results confirm the established notion that FGFR2 IIIB ligands (FGF7 and FGF10) are important for wound healing, they also suggest that decreased expression of multiple FGF ligands contributes to the slowing of wound healing in aged mice and indicate the potential importance of further study of the involvement of FGF9, 16, 18 and 23 in the wound healing process.

Cytogenetics, Immunostaining for Fibroblast Growth Factors, p53 Sequencing, and Clinical Features of Two Cases of Cystosarcoma Phyllodes

2000 ◽  
Vol 5 (3) ◽  
pp. 179-190 ◽  
Author(s):  
PAUL V. WOOLLEY ◽  
SUSANNE M. GOLLIN ◽  
WAHEEB RISKALLA ◽  
SYDNEY FINKELSTEIN ◽  
DAVID F. STEFANIK ◽  
...  
Keyword(s):  
Growth Factors ◽  
Clinical Features ◽  
Fibroblast Growth Factors ◽  
Fibroblast Growth ◽  
Cystosarcoma Phyllodes

Implications of Fibroblast Growth Factors (FGFs) in Cancer: From Prognostic to Therapeutic Applications

2019 ◽  
Vol 20 (8) ◽  
pp. 852-870
Author(s):  
Hassan Dianat-Moghadam ◽  
Ladan Teimoori-Toolabi
Keyword(s):  
Growth Factors ◽  
Wound Repair ◽  
Fibroblast Growth Factors ◽  
Predictive Biomarkers ◽  
Fibroblast Growth ◽  
Loss Of Function ◽  
Cellular Processes ◽  
Fgfr Signaling ◽  
Proliferation And Metastasis ◽  
Immense Potential

Fibroblast growth factors (FGFs) are pleiotropic molecules exerting autocrine, intracrine and paracrine functions via activating four tyrosine kinase FGF receptors (FGFR), which further trigger a variety of cellular processes including angiogenesis, evasion from apoptosis, bone formation, embryogenesis, wound repair and homeostasis. Four major mechanisms including angiogenesis, inflammation, cell proliferation, and metastasis are active in FGF/FGFR-driven tumors. Furthermore, gain-of-function or loss-of-function in FGFRs1-4 which is due to amplification, fusions, mutations, and changes in tumor–stromal cells interactions, is associated with the development and progression of cancer. Although, the developed small molecule or antibodies targeting FGFR signaling offer immense potential for cancer therapy, emergence of drug resistance, activation of compensatory pathways and systemic toxicity of modulators are bottlenecks in clinical application of anti-FGFRs. In this review, we present FGF/FGFR structure and the mechanisms of its function, as well as cross-talks with other nodes and/or signaling pathways. We describe deregulation of FGF/FGFR-related mechanisms in human disease and tumor progression leading to the presentation of emerging therapeutic approaches, resistance to FGFR targeting, and clinical potentials of individual FGF family in several human cancers. Additionally, the underlying biological mechanisms of FGF/FGFR signaling, besides several attempts to develop predictive biomarkers and combination therapies for different cancers have been explored.

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