Evidence map›Paper›PMID 24068256›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2014

Function of matrix IGF-1 in coupling bone resorption and formation.

Janet L Crane, Xu Cao

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
5.1field-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

73 citing papers in PubMed, 128 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Contribution of insulin‑like growth factor‑1 to tendon repair (Review).International journal of molecular medicine · 2025
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Chordoma cells possess bone-dissolving activity at the bone invasion front.Cellular oncology (Dordrecht, Netherlands) · 2024
    Article
  16. Bone-muscle crosstalk under physiological and pathological conditions.Cellular and molecular life sciences : CMLS · 2024
    Review
  17. Article
  18. Review
  19. Review
  20. Article

13 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Janet L CraneDepartment of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Ross Building, Room 229, 720 Rutland Ave, Baltimore, MD, 21205, USA, jcrane2@jhmi.edu.
Xu Cao
Johns Hopkins Medicine · US

Funding

JHU-UMD Diabetes Research CenterP30DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI AHIMA, REXFORD S. · 2013 to 2017
$9.7M
Interdepartmental Training Program in Cellular and Molecular EndocrinologyT32DK007751 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI WOLFE, ANDREW M · 1997 to 2016
$4.6M
MECHANISM OF SMAD1 MEDIATED OSTEOBLAST DIFFERENTIATIONR01DK057501 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CAO, XU · 2001 to 2014
$3.8M
TGF-beta Activity in the Subchondral Bone and Onset of OAR01AR063943 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI CAO, XU · 2013 to 2017
$2.2M
FUNCTION OF DNA VIRUS GENOMES IN ANIMAL CELLSZ01DK057501 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI OWENS, ROLAND ARVEL · 1986 to 2008
$846k
Intramural NIH HHS Z01 DK057501NIAMS NIH HHS AR063943NIAMS NIH HHS R01 AR063943NIDDK NIH HHS DK057501NIDDK NIH HHS P30 DK079637NIDDK NIH HHS R01 DK057501NIDDK NIH HHS T32 DK007751NIDDK NIH HHS T32DK007751
6 · The paper itself

Abstract

Balancing bone resorption and formation is the quintessential component for the prevention of osteoporosis. Signals that determine the recruitment, replication, differentiation, function, and apoptosis of osteoblasts and osteoclasts direct bone remodeling and determine whether bone tissue is gained, lost, or balanced. Therefore, understanding the signaling pathways involved in the coupling process will help develop further targets for osteoporosis therapy, by blocking bone resorption or enhancing bone formation in a space- and time-dependent manner. Insulin-like growth factor type 1 (IGF-1) has long been known to play a role in bone strength. It is one of the most abundant substances in the bone matrix, circulates systemically and is secreted locally, and has a direct relationship with bone mineral density. Recent data has helped further our understanding of the direct role of IGF-1 signaling in coupling bone remodeling which will be discussed in this review. The bone marrow microenvironment plays a critical role in the fate of mesenchymal stem cells and hematopoietic stem cells and thus how IGF-1 interacts with other factors in the microenvironment are equally important. While previous clinical trials with IGF-1 administration have been unsuccessful at enhancing bone formation, advances in basic science studies have provided insight into further mechanisms that should be considered for future trials. Additional basic science studies dissecting the regulation and the function of matrix IGF-1 in modeling and remodeling will continue to provide further insight for future directions for anabolic therapies for osteoporosis.

Indexed as

Bone RemodelingBone ResorptionHumansInsulin-Like Growth Factor IModels, BiologicalOsteoblastsOsteoclastsOsteogenesisOsteoporosisSignal TransductionInsulin-Like Growth Factor I

Identifiers

PMID24068256
PMCPMC3946714
OpenAlexW1978750436

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.