Evidence map›Paper›PMID 18304028›Full record

ReviewCritical reviews in eukaryotic gene expression2008

Regulation of chondrocytic gene expression by biomechanical signals.

Thomas J Knobloch, Shashi Madhavan, Jin Nam, Suresh Agarwal, Sudha Agarwal

Abstract readReview
In one paragraph

Review in Critical reviews in eukaryotic gene expression, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 70 citations in OpenAlex.

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  20. New developments in the treatment of osteoarthritis - focus on biologic agents.Open access rheumatology : research and reviews · 2015
    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

5 authors at 2 institutions in 1 country.

Thomas J KnoblochBiomechanics and Tissue Engineering Laboratory, Section of Oral Biology, Ohio State University College of Dentistry, 305 West 12th Avenue, Columbus, OH 43210, USA.
Shashi Madhavan
Jin Nam
Suresh Agarwal
Sudha Agarwal
Boston University · USThe Ohio State University · US

Funding

Exercise Driven Molecular Mechanisms of Joint RepairR01AR048781 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AGARWAL, SUDHA · 2002 to 2006
$1.5M
Inflammation of TMJDs: Role of Biomechanical SignalsR01DE015399 · NIDCR · OHIO STATE UNIVERSITY · PI AGARWAL, SUDHA · 2003 to 2006
$1.4M
STRESS-INDUCED ANTI-INFLAMMATORY SIGNALS IN CHONDROCYTESR01AT000646 · NCCIH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AGARWAL, SUDHA · 2000 to 2004
$1.1M
Physical Therapy, An Antiflammatory Signal on ArthritisR21HD040939 · NICHD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AGARWAL, SUDHA · 2001 to 2004
$655k
NCCIH NIH HHS AT 00646NCCIH NIH HHS R01 AT000646NIAMS NIH HHS AR 04878NIAMS NIH HHS R01 AR048781NICHD NIH HHS HD 40939NICHD NIH HHS R21 HD040939NIDCR NIH HHS DE 15399NIDCR NIH HHS R01 DE015399
6 · The paper itself

Abstract

Cartilage is a mechanosensitive tissue, which means that it can perceive and respond to biomechanical signals. Despite the known importance of biomechanical signals in the etiopathogenesis of arthritic diseases and their effectiveness in joint restoration, little is understood about their actions at the cellular level. Recent molecular approaches have revealed that specific biomechanical stimuli and cell interactions generate intracellular signals that are powerful inducers or suppressors of proinflammatory and reparative genes in chondrocytes. Biomechanical signals are perceived by cartilage in magnitude-, frequency-, and time-dependent manners. Static and dynamic biomechanical forces of high magnitudes induce proinflammatory genes and inhibit matrix synthesis. Contrarily, dynamic biomechanical signals of low/physiologic magnitudes are potent antiinflammatory signals that inhibit interleukin-1beta (IL-1beta)-induced proinflammatory gene transcription and abrogate IL-1beta/tumor necrosis factor-alpha-induced inhibition of matrix synthesis. Recent studies have identified nuclear factor-kB (NF-kB) transcription factors as key regulators of biomechanical signal-mediated proinflammatory and antiinflammatory actions. These signals intercept multiple steps in the NF-kappaB signaling cascade to regulate cytokine gene expression. Taken together, these findings provide insight into how biomechanical signals regulate inflammatory and reparative gene transcription, underscoring their potential in enhancing the ability of chondrocytes to curb inflammation in diseased joints.

Indexed as

Gene Expression RegulationAnimalsBiomechanical PhenomenaCartilageChondrocytesHumansInflammationInflammation MediatorsMechanotransduction, CellularModels, BiologicalNF-kappa BRegenerationTranscription, GeneticWounds and InjuriesInflammation MediatorsNF-kappa B

Identifiers

PMID18304028
PMCPMC4967411
OpenAlexW2016892864

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.