Biochemical and biophysical research communications · 2026
TGF-β1 promotes fibrosis of the ligamentum flavum by inducing FGF-2 release and activating the P38 MAPK pathway to regulate collagen synthesis.
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Lu Qilin, Ye Yuhui, Xie Tian, Wang Xiaozhen, Chen Long, Xi Jintao, Yang Kai
Аннотация
BACKGROUND: Ligamentum flavum hypertrophy (LFH) is a primary pathogenic factor of lumbar spinal canal stenosis (LSCS), characterized by fibroblast proliferation and extracellular matrix (ECM) remodeling. While transforming growth factor-β1 (TGF-β1) is a key regulator of LF fibrosis, its downstream signaling mechanisms remain unclear. This study investigated the role of the fibroblast growth factor-2 (FGF-2)/p38 mitogen-activated protein kinase (p38 MAPK) signaling axis downstream of TGF-β1 in LF fibrosis.
METHODS: LF tissues from patients with LSCS and lumbar disc herniation (LDH) were collected and assessed for TGF-β1, FGF-2, and p38 MAPK expression. Primary LF cells were cultured to establish a TGF-β1-induced fibrosis model. FGF-2 secretion, cell proliferation, and collagen (COL) expression were evaluated using ELISA, CCK-8, RT-qPCR, and Western blot. FGF-2 neutralizing antibodies and the p38 MAPK inhibitor SB203580 were used to verify the downstream mechanism.
RESULTS: TGF-β1, FGF-2, and p-p38 were significantly elevated in LSCS tissues compared to LDH controls. In vitro, TGF-β1 induced time-dependent FGF-2 secretion, promoted LF cell proliferation, and upregulated COL-I and COL-III, while these effects were significantly attenuated by FGF-2 neutralization. FGF-2 enhanced p38 MAPK phosphorylation and fibrotic marker expression, which were effectively blocked by SB203580. Collectively, these findings suggest that TGF-β1 promotes LF fibrosis by inducing FGF-2 expression and activating the p38 MAPK signaling pathway.
CONCLUSIONS: TGF-β1 promotes LF cell proliferation and ECM remodeling by upregulating FGF-2 expression and activating the p38 MAPK pathway, thereby synergistically driving the progression of LF fibrosis.
METHODS: LF tissues from patients with LSCS and lumbar disc herniation (LDH) were collected and assessed for TGF-β1, FGF-2, and p38 MAPK expression. Primary LF cells were cultured to establish a TGF-β1-induced fibrosis model. FGF-2 secretion, cell proliferation, and collagen (COL) expression were evaluated using ELISA, CCK-8, RT-qPCR, and Western blot. FGF-2 neutralizing antibodies and the p38 MAPK inhibitor SB203580 were used to verify the downstream mechanism.
RESULTS: TGF-β1, FGF-2, and p-p38 were significantly elevated in LSCS tissues compared to LDH controls. In vitro, TGF-β1 induced time-dependent FGF-2 secretion, promoted LF cell proliferation, and upregulated COL-I and COL-III, while these effects were significantly attenuated by FGF-2 neutralization. FGF-2 enhanced p38 MAPK phosphorylation and fibrotic marker expression, which were effectively blocked by SB203580. Collectively, these findings suggest that TGF-β1 promotes LF fibrosis by inducing FGF-2 expression and activating the p38 MAPK signaling pathway.
CONCLUSIONS: TGF-β1 promotes LF cell proliferation and ECM remodeling by upregulating FGF-2 expression and activating the p38 MAPK pathway, thereby synergistically driving the progression of LF fibrosis.