ArticlePloS one2011
Decreased bone formation and osteopenia in lamin a/c-deficient mice.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 72 citations in OpenAlex.
- In Vivo Base Editing Partially Rescues Bone Dysplasia in a Mouse Model of Hutchinson-Gilford Progeria Syndrome.Aging cell · 2026Article
- Murine Progeria Model Exhibits Delayed Fracture Healing With Senescent Phenotype and Dysregulated Immune Response.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026Article
- Wnt-presenting materials sustain H3K14-acetylation in human skeletal stem cells for tissue engineering and bone repair.NPJ Regenerative medicine · 2026Article
- Downregulation of Nesprin1 by Runx2 deficiency is critical for the development of skeletal laminopathy-like pathology.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Normal Bone Matrix Mineralization but Altered Growth Plate Morphology in the LmnaAging and disease · 2024Article
- Vasorin-deficient mice display disturbed vitamin D and mineral homeostasis in combination with a low bone mass phenotype.Bone reports · 2024Article
- Skeletal phenotypes and molecular mechanisms in aging mice.Zoological research · 2024Review
- Bone dysplasia in Hutchinson-Gilford progeria syndrome is associated with dysregulated differentiation and function of bone cell populations.Aging cell · 2023Article
- "Bone-SASP" in Skeletal Aging.Calcified tissue international · 2023Review
- The Senolytic Drug Fisetin Attenuates Bone Degeneration in theJournal of osteoporosis · 2023Article
- Overview of cellular homeostasis-associated nuclear envelope lamins and associated input signals.Frontiers in cell and developmental biology · 2023Review
- Matrix remodeling controls a nuclear lamin A/C-emerin network that directs Wnt-regulated stem cell fate.Developmental cell · 2022Article
- Review
- Review
- Lamin A/C Is Dispensable to Mechanical Repression of Adipogenesis.International journal of molecular sciences · 2021Article
- Steering cell behavior through mechanobiology in 3D: A regenerative medicine perspective.Biomaterials · 2021Review
- Nuclear mechanosensing controls MSC osteogenic potential through HDAC epigenetic remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Linking skeletal muscle aging with osteoporosis by lamin A/C deficiency.PLoS biology · 2020Article
- Review
- Lamin A/C Mechanotransduction in Laminopathies.Cells · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related bone loss is associated with changes in bone cellularity with characteristically low levels of osteoblastogenesis. The mechanisms that explain these changes remain unclear. Although recent in vitro evidence has suggested a new role for proteins of the nuclear envelope in osteoblastogenesis, the role of these proteins in bone cells differentiation and bone metabolism in vivo remains unknown. In this study, we used the lamin A/C null (Lmna⁻/⁻) mice to identify the role of lamin A/C in bone turnover and bone structure in vivo. At three weeks of age, histological and micro computed tomography measurements of femurs in Lmna⁻/⁻ mice revealed a significant decrease in bone mass and microarchitecture in Lmna⁻/⁻ mice as compared with their wild type littermates. Furthermore, quantification of cell numbers after normalization with bone surface revealed a significant reduction in osteoblast and osteocyte numbers in Lmna⁻/⁻ mice compared with their WT littermates. In addition, Lmna⁻/⁻ mice have significantly lower osteoclast number, which show aberrant changes in their shape and size. Finally, mechanistic analysis demonstrated that absence of lamin A/C is associated with increase expression of MAN-1 a protein of the nuclear envelope closely regulated by lamin A/C, which also colocalizes with Runx2 thus affecting its capacity as osteogenic transcription factor. In summary, these data clearly indicate that the presence of lamin A/C is necessary for normal bone turnover in vivo and that absence of lamin A/C induces low bone turnover osteopenia resembling the cellular changes of age-related bone loss.
Indexed as
Identifiers
What OpenQuestion holds
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.