ArticleBone2015
Follistatin-like 3 is a mediator of exercise-driven bone formation and strengthening.
Article in Bone, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Integrative multi-omics analysis deciphers the regulatory mechanisms of egg weight traits in chickens.Poultry science · 2025Article
- Integrated analysis of shared gene expression signatures and immune microenvironment heterogeneity in type 2 diabetes mellitus and colorectal cancer.Scientific reports · 2025Article
- FSTL3 is associated with prognosis and immune cell infiltration in lung adenocarcinoma.Journal of cancer research and clinical oncology · 2024Article
- Article
- Exercise maintains bone homeostasis by promoting osteogenesis through STAT3.International journal of biological sciences · 2023Article
- Roles of follistatin-like protein 3 in human non-tumor pathophysiologies and cancers.Frontiers in cell and developmental biology · 2022Review
- The Roles of Long-Term Hyperhomocysteinemia and Micronutrient Supplementation in theFrontiers in aging neuroscience · 2022Article
- Intermittent Hypoxic Therapy Inhibits Allogenic Bone-Graft Resorption by Inhibition of Osteoclastogenesis in a Mouse Model.International journal of molecular sciences · 2021Article
- Follistatin-Like Proteins: Structure, Functions and Biomedical Importance.Biomedicines · 2021Review
- Muscle, Bone, and Fat Crosstalk: the Biological Role of Myokines, Osteokines, and Adipokines.Current osteoporosis reports · 2020Review
- A comparative study on normal and obese mice indicates that the secretome of mesenchymal stromal cells is influenced by tissue environment and physiopathological conditions.Cell communication and signaling : CCS · 2020Article
- Physical Activity-Dependent Regulation of Parathyroid Hormone and Calcium-Phosphorous Metabolism.International journal of molecular sciences · 2020Review
- Up-Regulation of FSTL3, Regulated by lncRNA DSCAM-AS1/miR-122-5p Axis, Promotes Proliferation and Migration of Non-Small Cell Lung Cancer Cells.OncoTargets and therapy · 2020Article
- Physical Activity and Bone Health: What Is the Role of Immune System? A Narrative Review of the Third Way.Frontiers in endocrinology · 2019Review
- Strength Training Session Induces Important Changes on Physiological, Immunological, and Inflammatory Biomarkers.Journal of immunology research · 2018Article
- Mechanosensitive miRNAs and Bone Formation.International journal of molecular sciences · 2017Review
- Review
- Follistatin-like 3 suppresses cell proliferation and fibronectin expression via p38MAPK pathway in rat mesangial cells cultured under high glucose.International journal of clinical and experimental medicine · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 5 institutions in 1 country.
Funding
Abstract
Exercise is vital for maintaining bone strength and architecture. Follistatin-like 3 (FSTL3), a member of follistatin family, is a mechanosensitive protein upregulated in response to exercise and is involved in regulating musculoskeletal health. Here, we investigated the potential role of FSTL3 in exercise-driven bone remodeling. Exercise-dependent regulation of bone structure and functions was compared in mice with global Fstl3 gene deletion (Fstl3-/-) and their age-matched Fstl3+/+ littermates. Mice were exercised by low-intensity treadmill walking. The mechanical properties and mineralization were determined by μCT, three-point bending test and sequential incorporation of calcein and alizarin complexone. ELISA, Western-blot analysis and qRT-PCR were used to analyze the regulation of FSTL3 and associated molecules in the serum specimens and tissues. Daily exercise significantly increased circulating FSTL3 levels in mice, rats and humans. Compared to age-matched littermates, Fstl3-/- mice exhibited significantly lower fracture tolerance, having greater stiffness, but lower strain at fracture and yield energy. Furthermore, increased levels of circulating FSTL3 in young mice paralleled greater strain at fracture compared to the lower levels of FSTL3 in older mice. More significantly, Fstl3-/- mice exhibited loss of mechanosensitivity and irresponsiveness to exercise-dependent bone formation as compared to their Fstl3+/+ littermates. In addition, FSTL3 gene deletion resulted in loss of exercise-dependent sclerostin regulation in osteocytes and osteoblasts, as compared to Fstl3+/+ osteocytes and osteoblasts, in vivo and in vitro. The data identify FSTL3 as a critical mediator of exercise-dependent bone formation and strengthening and point to its potential role in bone health and in musculoskeletal diseases.
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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.