ArticleJournal of cellular and molecular medicine2023
Fibroblast growth factor 5 protects against spinal cord injury through activating AMPK pathway.
Article in Journal of cellular and molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Risk Assessment of Serum Biomarkers with Perioperative Neurocognitive Dysfunction in Elderly Patients Undergoing Thoracic Surgery: A Prospective Cohort Study.Cellular and molecular neurobiology · 2025Article
- FGFs/FGFRs and neuroinflammatory diseases: mechanism, drug therapies and delivery systems.Journal of advanced research · 2025Review
- Multi-Omic Analysis Reveals Genetic Determinants and Therapeutic Targets of Chronic Kidney Disease and Kidney Function.International journal of molecular sciences · 2024Article
- Genetically predicted inflammatory proteins and the risk of atrial fibrillation: a bidirectional Mendelian randomization study.Frontiers in cardiovascular medicine · 2024Article
- Fibroblast growth factor 5 protects against spinal cord injury through activating AMPK pathway.Journal of cellular and molecular medicine · 2023Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Excessive productions of inflammatory cytokines and free radicals are involved in spinal cord injury (SCI). Fibroblast growth factor 5 (FGF5) is associated with inflammatory response and oxidative damage, and we herein intend to determine its function in SCI. Lentivirus was instilled to overexpress or knockdown FGF5 expression in mice. Compound C or H89 2HCl were used to suppress AMP-activated protein kinase (AMPK) or protein kinase A (PKA), respectively. FGF5 level was significantly decreased during SCI. FGF5 overexpression mitigated, while FGF5 silence further facilitated inflammatory response, oxidative damage and SCI. Mechanically, FGF5 activated AMPK to attenuate SCI in a cAMP/PKA-dependent manner, while inhibiting AMPK or PKA with pharmacological methods significantly abolished the neuroprotective effects of FGF5 against SCI. More importantly, serum FGF5 level was decreased in SCI patients, and elevated serum FGF5 level often indicate better prognosis. Our study identifies FGF5 as an effective therapeutic and prognostic target for SCI.
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Registered trials
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