ArticlePloS one2014
Role of calcitonin gene-related peptide in functional adaptation of the skeleton.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Methodological aspects ofJournal of musculoskeletal & neuronal interactions · 2023Pooled it
- Calcitonin Gene-Related Peptide (CGRP) in Bone Repair and Musculoskeletal Pain: A Scoping Review of Skeletal Regeneration, Joint and Tendon Involvement, and CGRP-Targeted Therapies.Calcified tissue international · 2026Article
- Assessment of Bone Mineral Density Over 1 Year in a Cross-Sectional Cohort of Migraine Patients Receiving Anti-CGRP Monoclonal Antibodies.CNS drugs · 2024Article
- Sensory innervation in the prostate and a role for calcitonin gene-related peptide in prostatic epithelial proliferation.Frontiers in molecular neuroscience · 2024Article
- Ten open questions in migraine prophylaxis with monoclonal antibodies blocking the calcitonin-gene related peptide pathway: a narrative review.The journal of headache and pain · 2023Review
- Bone-to-Brain: A Round Trip in the Adaptation to Mechanical Stimuli.Frontiers in physiology · 2021Review
- The Effects of Calcitonin Gene-Related Peptide on Bone Homeostasis and Regeneration.Current osteoporosis reports · 2020Review
- No pain, no gain? The effects of pain-promoting neuropeptides and neurotrophins on fracture healing.Bone · 2020Review
- Calcitonin and Bone Physiology: In Vitro, In Vivo, and Clinical Investigations.International journal of endocrinology · 2020Review
- Fracture repair requires TrkA signaling by skeletal sensory nerves.The Journal of clinical investigation · 2019Article
- Calcitonin gene-related peptide enhances osteogenic differentiation and recruitment of bone marrow mesenchymal stem cells in rats.Experimental and therapeutic medicine · 2019Article
- Sensory Neuropeptides and their Receptors Participate in Mechano-Regulation of Murine Macrophages.International journal of molecular sciences · 2019Article
- Temporal mechanically-induced signaling events in bone and dorsal root ganglion neurons after in vivo bone loading.PloS one · 2018Article
- NGF-TrkA signaling in sensory nerves is required for skeletal adaptation to mechanical loads in mice.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
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 1 institution in 1 country.
Funding
Abstract
Peptidergic sensory nerve fibers innervating bone and periosteum are rich in calcitonin gene-related peptide (CGRP), an osteoanabolic neurotransmitter. There are two CGRP isoforms, CGRPα and CGRPβ. Sensory fibers are a potential means by which the nervous system may detect and respond to loading events within the skeleton. However, the functional role of the nervous system in the response of bone to mechanical loading is unclear. We used the ulna end-loading model to induce an adaptive modeling response in CGRPα and CGRPβ knockout mouse lines and their respective wildtype controls. For each knockout mouse line, groups of mice were treated with cyclic loading or sham-loading of the right ulna. A third group of mice received brachial plexus anesthesia (BPA) of the loaded limb before mechanical loading. Fluorochrome labels were administered at the time of loading and 7 days later. Ten days after loading, bone responses were quantified morphometrically. We hypothesized that CGRP signaling is required for normal mechanosensing and associated load-induced bone formation. We found that mechanically-induced activation of periosteal mineralizing surface in mice and associated blocking with BPA were eliminated by knockout of CGRPα signaling. This effect was not evident in CGRPβ knockout mice. We also found that mineral apposition responses to mechanical loading and associated BPA blocking were retained with CGRPα deletion. We conclude that activation of periosteal mineralizing surfaces in response to mechanical loading of bone is CGRPα-dependent in vivo. This suggests that release of CGRP from sensory peptidergic fibers in periosteum and bone has a functional role in load-induced bone formation.
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.