FGF22

Last update 08 May 2025

Basic Info

Synonyms

FGF-22, FGF22, fibroblast growth factor 22

Introduction

Plays a role in the fasting response, glucose homeostasis, lipolysis and lipogenesis. Can stimulate cell proliferation (in vitro). May be involved in hair development.

100 Clinical Results associated with FGF22

100 Translational Medicine associated with FGF22

0 Patents (Medical) associated with FGF22

Literatures (Medical) associated with FGF22

01 Jun 2025·SLAS Technology

Identifcation of the FGF family as therapeutic targets and prognostic biomarkers in the microenvironment of head and neck squamous cell carcinoma

Article

Author: Wei, Jian ; Xu, Yingjiao ; Gao, Yingchun ; Zhang, Xuan ; Tian, Yumei ; Liu, Xuqian ; Nie, Minhai ; Zhang, Li

BACKGROUNDAlmost 90 % of head and neck malignancies are malignant squamous cell cancers, making it the sixth most common malignancy in the developing countries, with an overall five-year overall survival rate about 40 %-50 %. Early diagnosis and treatment can bring a better prognosis. Fibroblast growth factor (FGF) is an important polypeptide in vivo. Studies have found that FGF signal has carcinogenic potential and participates in a variety of carcinogenic behaviors. Some experiments have proved that FGF signal has the function of tumor inhibition in some cases, and the role of FGF signalling in tissue repair and homeostasis suggest a role for FGF in targeted therapy and prognosis. However, its manifestation and predictive role in HNSC have not been clearly defined.METHODSGenome-wide expression analysis of Oncomine evaluated the evaluation of FGF family expression in HNSC. Expression analysis and HNSC data set were used to obtain FGF family expression data and T statistic was applied for analysis. The differential mRNA expression levels in tumor versus normal tissues, as well as the correlation with pathological staging and prognosis, were examined using the GEPIA single-gene analysis tool for the FGF family.FGF family altered CO expression and network modules were obtained from cBioportal and analyzed in 520 HNSC samples.Pro-protein interaction (PPI) flow network is performed on the differentially ordered FGF clusters using STRING, Gene Operating System (GO) domain domain enrichment as well as Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis are performed on the FGF cluster and its neighbouring genes using DAVID6.8, key transcriptional factors (TF) of FGF family was analyzed by TRRUST, correlation between FGF family level and autoimmune cell migration was evaluated by TIMER, and biological analysis of FGF family kinase target enrichment was performed using LinkInterpreter.RESULTSOnly the expression of FGF6 in HNSC was down-regulated in all FGF family(FC=2),Transcriptional level of FGF1, FGF2, FGF5, FGF7-14, FGF17-19, FGF21 and FGF22 was upregulated in HNSC .In terms of the relative level of FGF family in HNSC, the greatest amount of FGF11. In different pathological stages of HNSC, the expression of FGF was meaningless (P>0.05), and FGF3-6, FGF8-10, FGF14, FGF16, FGF17, FGF1921, FGF23 showed no significant difference in different HNSC stages. Low expression of FGF5 and high expression of FGF22 had low overall survival(OS) rate of HNSC(P =0.012, P =0.0015). In addition, enrichment analysis of FGF family in HNSC showed that it was highly abundant in PI3K-Akt signaling pathway, MAPK and rasper pathway. Our data showed that ATF4, STAT, RELA, NFKB1 are key transcription target of the FGF family, NLK, LOCK1, LYN, ZAP70, MAP2K3, RPS6KA4, AURKB, ATR, ROCK1, MYLK2, CAMK2A, EGFR, MAPK3, MAP3K8, SYK, LCK, HCK, PKN2, RPS6KA1, BUB1, CDK5, ITK, FYN, TBK1, ATM, CDK2, PTK2 are kinase targets of the FGF family. We identified a relationship between the modulation of FGF expression and cellular infiltration, such as B lymphocytes, CD4+ T cells and macrophages dendritic cells.CONCLUSIONSOur data may shed new light on the choice of immunotherapeutic targets and predictive biomarkers in HNSC.

01 May 2025·Differentiation

Fibroblast growth factor 22

Article

Author: Furuta, Rise ; Miyake, Ayumi

Fibroblast growth factor 22 (FGF22) is a member of the FGF7 subfamily that functions as a paracrine factor and was identified in the human placenta in 2001. The FGF22 gene is located on human chromosome 19p13.3, mouse chromosome 10, and zebrafish chromosome 22 and is closely linked to the BSG, HCN2, and POLRMT genes. The gene is composed of three exons, which are common in humans, mice, and zebrafish. However, in humans and mice, FGF22 is produced as two isoforms by alternative splicing, whereas no isoforms have been reported in zebrafish. In humans, FGF22 is expressed in the skin, brain, and ovaries, whereas in mice, it is expressed in the skin, brain, retina, spinal cord, and cochlea. Various abnormalities have been reported in these regions in Fgf22 mutant mice. In zebrafish, fgf22 is expressed in the forebrain, midbrain, and otic vesicles during embryogenesis, and an analysis of knockdown zebrafish models revealed an important role for fgf22 in the process of brain formation. As expected from the results of these functional analyses, FGF22 is also associated with human diseases such as depression, spinal cord injury, hearing loss, and cancer.

01 Jan 2025·International Immunopharmacology

Pentraxin 3 promotes microglial M2 polarization and excitatory synapse formation in the hippocampus in depression

Article

Author: Yu, Ming ; Wang, Man ; Wei, Hong ; Li, Yuefeng ; Xu, Yuhao

Depression is a prevalent mental illness that significantly impairs individuals' overall quality of life and physical well-being. However, the pathological mechanisms of depression remain unclear, and effective treatment strategies are urgently needed. Pentraxin 3 (PTX3), a long pentraxin protein, plays a significant role in various pathological conditions, including infections, immune responses, and tissue repair. In this study, we collected serum from patients with depression and established both animal and cell models of depression. We found that PTX3 expression was significantly reduced in both the serum of patients with depression and the hippocampus of chronic unpredictable mild stress (CUMS) mice. PTX3 supplementation markedly improved depressive-like behavior in CUMS mice and promoted microglial M2 polarization. In the LPS-induced BV2 cell model, PTX3 overexpression facilitated microglial M2 polarization via activation of the CREB/CEBPb axis. Additionally, PTX3 enhanced fibroblast growth factor 22 (FGF22) expression and excitatory synapse formation in the CA3 region of the hippocampus in CUMS mice. In the dexamethasone (DXM)-treated SH-SY5Y cell model, PTX3 overexpression increased SPI1 expression, elevated FGF22 transcriptional activity, and promoted the expression of excitatory synapse-related proteins PSD95 and VGLUT1. In summary, our study demonstrates that PTX3 promotes microglial M2 polarization and excitatory synapse formation in the hippocampus, suggesting potential antidepressant effects and providing theoretical support for considering PTX3 as a therapeutic target for depression.

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FGF22

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