Department of Molecular Science and Technology, Ajou University, Suwon 16499, Korea.
S&K Therapeutics, Ajou University Campus Plaza 418, 199 Worldcup-ro, Yeongtong-gu, Suwon 16502, Korea.
Cells. 2021 Nov 19;10(11):3242. doi: 10.3390/cells10113242.
Fibroblast growth factors (FGFs) are a large family of secretory molecules that act through tyrosine kinase receptors known as FGF receptors. They play crucial roles in a wide variety of cellular functions, including cell proliferation, survival, metabolism, morphogenesis, and differentiation, as well as in tissue repair and regeneration. The signaling pathways regulated by FGFs include RAS/mitogen-activated protein kinase (MAPK), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)-protein kinase B (AKT), phospholipase C gamma (PLCγ), and signal transducer and activator of transcription (STAT). To date, 22 FGFs have been discovered, involved in different functions in the body. Several FGFs directly or indirectly interfere with repair during tissue regeneration, in addition to their critical functions in the maintenance of pluripotency and dedifferentiation of stem cells. In this review, we summarize the roles of FGFs in diverse cellular processes and shed light on the importance of FGF signaling in mechanisms of tissue repair and regeneration.
成纤维细胞生长因子(FGFs)是一大类分泌分子,通过酪氨酸激酶受体(即 FGF 受体)发挥作用。它们在多种细胞功能中发挥着关键作用,包括细胞增殖、存活、代谢、形态发生和分化,以及组织修复和再生。FGF 调节的信号通路包括 RAS/丝裂原活化蛋白激酶(MAPK)、磷脂酰肌醇-4,5-二磷酸 3-激酶(PI3K)-蛋白激酶 B(AKT)、磷脂酶 C 伽马(PLCγ)和信号转导子和转录激活子(STAT)。迄今为止,已经发现了 22 种 FGFs,它们参与了体内的不同功能。几种 FGFs 直接或间接地干扰组织再生过程中的修复,除了它们在维持多能性和干细胞去分化方面的关键作用。在这篇综述中,我们总结了 FGFs 在多种细胞过程中的作用,并阐明了 FGF 信号在组织修复和再生机制中的重要性。
Wiley Interdiscip Rev Dev Biol. 2015
Curr Drug Targets. 2021
Front Cell Dev Biol. 2020-2-18
Development. 2017-11-15
Endocr Relat Cancer. 2004-12
WIREs Mech Dis. 2022-7
Cells. 2021-7-20
Adv Mater Technol. 2025-7-9
Naunyn Schmiedebergs Arch Pharmacol. 2025-8-28
Ann Med Surg (Lond). 2025-7-16
Front Endocrinol (Lausanne). 2021
Front Cell Dev Biol. 2021-5-14
Cancer Gene Ther. 2021-9
Cancers (Basel). 2020-12-18