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Fibroblast Growth Factors
Published in Jason Kelley, Cytokines of the Lung, 2022
The fibroblast growth factors (FGFs) are a family of related mitogens that have proliferative and differentiative effects on a variety of cells. Although there are a few reports of the presence of the FGFs in lung tissue, and lung is often screened along with other tissues for expression of mRNAs for members of the FGF family, little is known about the role of FGFs in lung biology. Since the FGFs are potent mitogens for endothelial cells, fibroblasts, chondrocytes, and some epithelial cells, they have the potential to interact with the component tissues of the lung and may have profound effects on lung physiology. This review will outline the present knowledge about the biological and chemical properties of the FGFs and their receptors and will consider biological effects of the FGFs that may be relevant to lung biology.
Gene Therapy for Cardiovascular Diseases
Published in Yashwant Pathak, Gene Delivery, 2022
Dhwani Thakkar, Vandit Shah, Jigna Shah
Insufficient blood supply to the myocardium is caused by ischemic heart disease and atherosclerotic stenosis. The fundamental concept of angiogenesis and formation of blood vessels, which has already been addressed, can be used to cure this. Several growth factors, including fibroblast growth factor (FGF), vascular endothelial growth factor (VEGF), and hepatocyte growth factor (HGF), are employed in gene therapy procedures combined with cell treatment. Several clinical trials, such as APIRE63, AWARE, KAT 301,64 and many more as mentioned in Table 6.2, have been put into effect in the last 10 years using plasmid or adenovirus as a vector to achieve success. However, phase II/III trials have yielded no clinically relevant evidence yet.65 There are several new targets, such as thymosin B4, GalNac-antisense oligonucleotide, promoter activating siRNA, exosomes, and hypoxia inducible factor 1a, which help to target ischemic myocardium. However, currently no clinical trials are focusing on the new target for treatment.66
Urothelial and Urethral Cancer
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Ibrahim Jubber, Karl H. Pang, James W.F. Catto
FGFR3 mutationsActivate the FGF growth pathway.Associated with a favourable clinical phenotype (fewer progression and recurrence events).FGF-targeting small molecules are now entering clinical practice (e.g., erdafitinib is FDA approved).
Sprifermin: a recombinant human fibroblast growth factor 18 for the treatment of knee osteoarthritis
Published in Expert Opinion on Investigational Drugs, 2021
Jia Li, Xiaoshuai Wang, Guangfeng Ruan, Zhaohua Zhu, Changhai Ding
Fibroblast growth factor 18 (FGF18) was first identified and reported as a new member of the FGF family by Japanese researchers in 1998 [14]. They isolated the cDNA encoding FGF18 from rat embryos in the in vitro study, and then determined human FGF18 with high identity (99.0%) of amino acid to rat. The uniqueness of FGF18 mRNA in spatial pattern was finally distinguished from previously reported FGF-8 and FGF-17 mRNAs [14]. Subsequently, its gene was demonstrated mapping to human chromosome 5q34 and designated as Fgf18 by the Human Genome Organization, considering its potential clinical utility [15]. Human FGF18, which was mainly expressed in kidneys, lungs, and some discrete regions during embryologic development, belonged to FGF8 and FGF17 subfamily of FGFs [16]. It had a full length of 207 amino acids with two N-linked glycosylation domains [17]. It was well acknowledged that human FGF18 had critical roles in the physiological regulation of skeletal development, skin maintenance, hair growth, angiogenesis, neuronal activity, and morphogenesis [18–21]. Therefore, FGF 18 would have great pharmacological potentials in the treatment of human diseases.
Fibroblast Growth Factor Receptor Inhibitors Reduce Adipogenesis of Orbital Fibroblasts and Enhance Myofibroblastic Differentiation in Graves’ Orbitopathy
Published in Ocular Immunology and Inflammation, 2021
Shyang-Rong Shih, Shu-Lang Liao, Chih-Wei Shih, Yi-Hsuan Wei, Ting-Xuan Lu, Chien-Hsiang Chou, Er-Yen Yen, Yi-Cheng Chang, Chia-Chi Lin, Yu-Chiao Chi, Wei-Shiung Yang, Feng-Chiao Tsai
Evidence supports the involvement of thyroid-stimulating hormone (TSH) receptor (TSHR) and TSHR antibodies (TSHRAbs) in the pathogenesis of GO.6 Studies have also shown that insulin-like growth factor-1 (IGF-1) induces chemoattractants in orbital fibroblasts and IGF-1 receptor (IGF-1R) mediates the induction of GAG synthesis.6 IGF-1R targeting antibodies with or without TSHR antagonist have been introduced as new strategies for GO treatment and have undergone clinical trials.7,8 Fibroblast growth factors (FGFs) are also important growth factors. There are totally 22 FGFs and 4 FGF receptors (FGFRs). Binding of FGFs to FGFRs can induce the proliferation and differentiation of fibroblasts.9 FGF1 and FGF2 are thought to be key regulators of human adipogenesis.10,11 Previous studies have shown that FGF (type not specified) expression increased in retroocular connective tissue of GO; serum FGF2 increased in GO patients; and FGF2 induced adipogenesis, proliferation and cytokine/hyaruronon production of fibroblasts in GO.12–17 Details about FGF1 including serum levels and effects on orbital fibroblasts of GO were less discussed.
Pubertal growth in height, sitting height and leg length in achondroplasia
Published in Annals of Human Biology, 2021
T. J. Cole, M. del Pino, P. Adamo, V. Fano
Achondroplasia (ACH), an autosomal-dominant disorder, is the most common form of inherited disproportionate short stature, with a worldwide birth prevalence, based on meta-analysis, of 4.6 per 100,000 (Spranger 2012; Foreman et al. 2020). It is caused by a gain of function mutation in the type 3 fibroblast growth factor receptor gene (FGFR3) located on chromosome 4p16.3 (Shiang et al. 1994; Bellus et al. 1995). FGFR3 plays an important role in early mammalian skeletal development, especially in post-embryonic linear bone growth with an inhibition predominantly of endochondral ossification (Foldynova-Trantirkova et al. 2012; Qi et al. 2014). Consequently, children with ACH are born with shorter limbs than non-ACH children, and their limb deficit increases throughout childhood (del Pino et al. 2016; del Pino, Ramos Mejía, et al. 2018).