Evidence map›Paper›PMID 12023876›Full record

ReviewThe Biochemical journal2002

Mechanisms balancing skeletal matrix synthesis and degradation.

Harry C Blair, Mone Zaidi, Paul H Schlesinger

Open access · bronzeAbstract readReview
In one paragraph

Review in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.0field-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

38 citing papers in PubMed, 153 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
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  11. Review
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  13. Review
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  15. Review
  16. The atherogenic Scarb1 null mouse model shows a high bone mass phenotype.American journal of physiology. Endocrinology and metabolism · 2014
    Article
  17. Article
  18. Macrophage-stimulating protein and calcium homeostasis in zebrafish.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012
    Article
  19. Article
  20. Article
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 3 institutions in 1 country.

Harry C BlairDepartment of Pathology, University of Pittsburgh and Veteran's Affairs Health System, Pittsburgh, Pennsylvania, USA. hcblair@imap.pitt.edu
Mone Zaidi
Paul H Schlesinger
Geriatric Research Education and Clinical Center · USVA Pittsburgh Healthcare System · USWashington University in St. Louis · US

Funding

OSTEOCLAST REGULATION BY IONIZED CALCIUMR01AG014917 · NIA · UNIVERSITY OF PENNSYLVANIA · PI ZAIDI, MONE · 1997 to 2003
$1.4M
RUFFLED BORDER CHLORIDE CHANNEL: REGULATION AND CLONINGR01AR046539 · NIAMS · WASHINGTON UNIVERSITY · PI SCHLESINGER, PAUL H · 2001 to 2004
$1.1M
PHYTOESTROGEN REGULATION OF BONE TURNOVERR01AR047700 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BLAIR, HARRY C. · 2000 to 2004
$1.0M
CALMODULIN AND OSTEOCLAST CONTROLR01AG012951 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BLAIR, HARRY C. · 1994 to 2003
$858k
NIAMS NIH HHS AR46539NIAMS NIH HHS AR47700NIA NIH HHS AG12951NIA NIH HHS AG14917
6 · The paper itself

Abstract

Bone is regulated by evolutionarily conserved signals that balance continuous differentiation of bone matrix-producing cells against apoptosis and matrix removal. This is continued from embryogenesis, where the skeleton differentiates as a solid mass and is shaped into separate bones by cell death and proteolysis. The two major tissues of the skeleton are avascular cartilage, with an extracellular matrix based on type II collagen and hydrophilic proteoglycans, and bone, a stronger and lighter material based on oriented type I collagen and hydroxyapatite. Both differentiate from the same mesenchymal stem cells. This differentiation is regulated by a family of related signals centred on bone morphogenic proteins. Fibroblast growth factors, Indian hedgehog and parathyroid hormone-related protein are important in determining the type of matrix and the relation of skeletal and non-skeletal structures. Removal of mineralized matrix involves apoptosis of matrix cells and differentiation of acid-secreting cells (osteoclasts) from macrophage precursors. Key regulators of matrix removal are signals in the tumour-necrosis-factor family. Osteoclasts dissolve bone by isolating a region of the matrix and secreting HCl and proteinases at that site. Successive cycles of removal and replacement allow growth, repair and remodelling. The signals for bone turnover are predominantly cell-membrane-associated, allowing very specific spatial regulation. In addition to its support function, bone is a reservoir of Ca2+, PO3-(4) and OH-. Secondary modulation of mineral secretion and bone degradation are mediated by humoral signals, including parathyroid hormone and vitamin D, as well as the cytokines that also regulate the underlying cell differentiation.

Indexed as

Bone DevelopmentAnimalsApoptosisBone and BonesCell DifferentiationExtracellular MatrixHumansOsteoblastsOsteoclasts

Identifiers

PMID12023876
PMCPMC1222578
OpenAlexW2000011999

What OpenQuestion holds

Textmetadata
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.