Evidence map›Paper›PMID 26038304›Full record

ReviewReviews in endocrine & metabolic disorders2015

Physiological mechanisms and therapeutic potential of bone mechanosensing.

Zhousheng Xiao, Leigh Darryl Quarles

Abstract readReview
In one paragraph

Review in Reviews in endocrine & metabolic disorders, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  9. Fin ray branching is defined by TRAPProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Review
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  12. Article
  13. Mechanical loading activates the YAP/TAZ pathway and chemokine expression in the MLO-Y4 osteocyte-like cell line.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
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  20. The regulation of RANKL by mechanical force.Journal of bone and mineral metabolism · 2021
    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

2 authors at 1 institution in 1 country.

Zhousheng XiaoDepartment of Medicine, University of Tennessee Health Science Center, Memphis, TN, 38165, USA.
Leigh Darryl Quarles
University of Tennessee Health Science Center · US

Funding

DIFFERENTIAL FUNCTION AND REGULATION OF RUNX2 ISOFORMSR01AR049712 · NIAMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI QUARLES, L DARRYL · 2003 to 2007
$1.7M
Extrarenal Functions of Polycystin-1R01DK083303 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI QUARLES, L DARRYL · 2010 to 2014
$1.6M
NIAMS NIH HHS R01 AR049712NIDDK NIH HHS DK083303NIDDK NIH HHS R01 DK083303
6 · The paper itself

Abstract

Skeletal loading is an important physiological regulator of bone mass. Theoretically, mechanical forces or administration of drugs that activate bone mechanosensors would be a novel treatment for osteoporotic disorders, particularly age-related osteoporosis and other bone loss caused by skeletal unloading. Uncertainty regarding the identity of the molecular targets that sense and transduce mechanical forces in bone, however, has limited the therapeutic exploitation of mechanosesning pathways to control bone mass. Recently, two evolutionally conserved mechanosensing pathways have been shown to function as "physical environment" sensors in cells of the osteoblasts lineage. Indeed, polycystin-1 (Pkd1, or PC1) and polycystin-2 (Pkd2, or PC2' or TRPP2), which form a flow sensing receptor channel complex, and TAZ (transcriptional coactivator with PDZ-binding motif, or WWTR1), which responds to the extracellular matrix microenvironment act in concert to reciprocally regulate osteoblastogenesis and adipogenesis through co-activating Runx2 and a co-repressing PPARγ activities. Interactions of polycystins and TAZ with other putative mechanosensing mechanism, such as primary cilia, integrins and hemichannels, may create multifaceted mechanosensing networks in bone. Moreover, modulation of polycystins and TAZ interactions identify novel molecular targets to develop small molecules that mimic the effects of mechanical loading on bone.

Indexed as

Molecular Targeted TherapyAdipogenesisAnimalsBone and BonesCiliaHumansMechanotransduction, CellularOsteoblastsOsteoporosisTRPP Cation ChannelsWeight-BearingTRPP Cation Channels

Identifiers

PMID26038304
PMCPMC5079521
OpenAlexW635064942

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.