ArticleScientific reports2021
Gait disturbances and muscle dysfunction in fibroblast growth factor 2 knockout mice.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed, 12 citations in OpenAlex.
- Effects of fibroblast growth factor 2 on muscle precursor cells from mouse limb and extraocular muscle.PloS one · 2026Article
- The Relationship Between Grip Strength and Cognitive Impairment: Evidence From NHANES 2011-2014.Brain and behavior · 2025Article
- Exerkines and myokines in aging sarcopenia.Frontiers in endocrinology · 2025Review
- Role of signaling pathways in age-related orthopedic diseases: focus on the fibroblast growth factor family.Military Medical Research · 2024Review
- DNA methylation of skeletal muscle function-related secretary factors identifies FGF2 as a potential biomarker for sarcopenia.Journal of cachexia, sarcopenia and muscle · 2024Article
- Exploring the Intricate Nexus of Sarcopenia and Cognitive Impairment.Aging and disease · 2023Review
- The function of previously unappreciated exerkines secreted by muscle in regulation of neurodegenerative diseases.Frontiers in molecular neuroscience · 2023Review
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Fibroblast growth factor 2 (FGF2) is important in musculoskeletal homeostasis, therefore the impact of reduction or Fgf2 knockout on skeletal muscle function and phenotype was determined. Gait analysis as well as muscle strength testing in young and old WT and Fgf2KO demonstrated age-related gait disturbances and reduction in muscle strength that were exacerbated in the KO condition. Fgf2 mRNA and protein were significantly decreased in skeletal muscle of old WT compared with young WT. Muscle fiber cross-sectional area was significantly reduced with increased fibrosis and inflammatory infiltrates in old WT and Fgf2KO vs. young WT. Inflammatory cells were further significantly increased in old Fgf2KO compared with old WT. Lipid-related genes and intramuscular fat was increased in old WT and old Fgf2KO with a further increase in fibro-adipocytes in old Fgf2KO compared with old WT. Impaired FGF signaling including Increased β-Klotho, Fgf21 mRNA, FGF21 protein, phosphorylated FGF receptors 1 and 3, was observed in old WT and old Fgf2KO. MAPK/ ERK1/2 was significantly increased in young and old Fgf2KO. We conclude that Fgf2KO, age-related decreased FGF2 in WT mice, and increased FGF21 in the setting of impaired Fgf2 expression likely contribute to impaired skeletal muscle function and sarcopenia in mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.