Evidence map›Paper›PMID 28980721›Full record

ReviewJournal of orthopaedic research : official publication of the Orthopaedic Research Society2018

IGF-1 signaling mediated cell-specific skeletal mechano-transduction.

Faming Tian, Yongmei Wang, Daniel D Bikle

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Consequences of Aging on Bone.Aging and disease · 2023
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Interaction between diabetes and osteoporosis: imbalance between inflammation and bone remodeling.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Conditional Loss of Nmp4 in Mesenchymal Stem Progenitor Cells Enhances PTH-Induced Bone Formation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023
    Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Faming TianEndocrine Research Unit, Department of Medicine, University of California San Francisco and VA Medical Center, 1700 Owens St, San Francisco, 94158, CA.
Yongmei WangEndocrine Research Unit, Department of Medicine, University of California San Francisco and VA Medical Center, 1700 Owens St, San Francisco, 94158, CA.
Daniel D BikleEndocrine Research Unit, Department of Medicine, University of California San Francisco and VA Medical Center, 1700 Owens St, San Francisco, 94158, CA.
San Francisco VA Medical Center · USUniversity of California, San Francisco · US

Funding

Role of IGF-I/integrin signaling in the periosteal response to loadR01AR055924 · NIAMS · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI BIKLE, DANIEL DAVID · 2008 to 2019
$3.5M
UCSF Core Center for Musculoskeletal Biology and MedicineP30AR066262 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MAJUMDAR, SHARMILA · 2014 to 2018
$3.0M
Mechanisms Underlying Hormonal Regulation of Fracture RepairIP1BX001599 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI BIKLE, DANIEL DAVID, NISSENSON, ROBERT · 2012 to 2015
–
BLRD VA IP1 BX001599NIAMS NIH HHS P30 AR066262NIAMS NIH HHS R01 AR055924
6 · The paper itself

Abstract

Mechanical loading preserves bone mass and stimulates bone formation, whereas skeletal unloading leads to bone loss. In addition to osteocytes, which are considered the primary sensor of mechanical load, osteoblasts, and bone specific mesenchymal stem cells also are involved. The skeletal response to mechanical signals is a complex process regulated by multiple signaling pathways including that of insulin-like growth factor-1 (IGF-1). Conditional osteocyte deletion of IGF-1 ablates the osteogenic response to mechanical loading. Similarly, osteocyte IGF-1 receptor (IGF-1R) expression is necessary for reloading-induced periosteal bone formation. Transgenic overexpression of IGF-1 in osteoblasts results in enhanced responsiveness to in vivo mechanical loading in mice, a response which is eliminated by osteoblastic conditional disruption of IGF-1 in vivo. Bone marrow derived stem cells (BMSC) from unloaded bone fail to respond to IGF-1 in vitro. IGF-1R is required for the transduction of a mechanical stimulus to downstream effectors, transduction which is lost when the IGF-1R is deleted. Although the molecular mechanisms are not yet fully elucidated, the IGF signaling pathway and its interactions with potentially interlinked signaling cascades involving integrins, the estrogen receptor, and wnt/β-catenin play an important role in regulating adaptive response of cancer bone cells to mechanical stimuli. In this review, we discuss recent advances investigating how IGF-1 and other interlinked molecules and signaling pathways regulate skeletal mechano-transduction involving different bone cells, providing an overview of the IGF-1 signaling mediated cell-specific response to mechanical stimuli. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:576-583, 2018.

Indexed as

Mechanotransduction, CellularAnimalsBone and BonesInsulin-Like Growth Factor IMesenchymal Stem CellsOsteocytesSignal TransductionInsulin-Like Growth Factor IIGF-1IGF-1 receptormechanical stimulimesenchymal stem cellsosteoblastsosteocytes

Identifiers

PMID28980721
PMCPMC5839951
OpenAlexW2761905440

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.