Table 2.

Changes in the level of expression of members of the fibroblast growth factor (FGF) family in disease

FGF	Changes	Effect	Reference
Intervertebral disc disease
FGF2	Increased	Low concentration of FGF2 activates the mitogen-activated extracellular signal-regulated kinase (MEK)-extracellular signal-regulated kinase (ERK) and phosphatidylinositol-3-kinase - protein kinase B (Akt) pathways and promotes the proliferation of NP and AF cells; Promote fibrocartilage synthesis	[142, 143]
FGF18	Decreased	Promote cartilage synthesis; Inhibit cartilage catabolism	[11, 144]
Osteoporosis
FGF2	Decreased	Promote parathyroid hormone -mediated bone anabolic metabolism through the Wnt/β-catenin signaling pathway and maintains calcium phosphate homeostasis to promote bone growth, development, and fracture healing	[145]
FGF19	Decreased	Regulate glucose and lipid metabolism and bile acid metabolism, and activate the Wnt/β-catenin signaling pathway, promote osteoblast differentiation, inhibit osteoclast generation	[146, 147]
FGF21	Increased	Improve glucose and lipid metabolism, indirectly affecting bone mass	[8, 148]
FGF23	Increased	Regulate calcium and phosphorus metabolism and reduce bone formation	[149, 150]
Sarcopenia
FGF2	Increased	Increase muscle mass and promote intramuscular adipose tissue	[151–153]
FGF19	Decreased	Improve muscle glucose and lipid metabolism and promote muscle growth	[154, 155]
FGF21	Increased	Promote muscle cell growth by activating the ERK1/2 signaling pathway and ribosomal protein S6 kinase 1 (S6K1) and improve systemic metabolism and reduce muscle mass	[156, 157]
FGF23	Increased	Promote aging of muscle and stem cells	[158, 159]