Evidence map›Paper›PMID 33086121›Full record

ReviewLife sciences2020

Role of mitochondria in mediating chondrocyte response to mechanical stimuli.

Yuchen He, Meagan J Makarczyk, Hang Lin

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Life sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

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  14. Mechanism of ERK/CREB pathway in pain and analgesia.Frontiers in molecular neuroscience · 2023
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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 1 country.

Yuchen HeDepartment of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA, United States of America.
Meagan J MakarczykDepartment of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA, United States of America; Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, United States of America.
Hang LinDepartment of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA, United States of America; Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, United States of America; McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, United States of America. Electronic address: hal46@pitt.edu.
University of Pittsburgh · USMcGowan Institute for Regenerative Medicine · US

Funding

Joint Pain on a Chip: Mechanistic Analysis Therapeutic Targets and an Empirical Strategy for Personalized Pain ManagementUG3TR003090 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GOLD, MICHAEL S, LIN, HANG · 2019 to 2019
$1.5M
NCATS NIH HHS UG3 TR003090
6 · The paper itself

Abstract

As the most common form of arthritis, osteoarthritis (OA) has become a major cause of severe joint pain, physical disability, and quality of life impairment in the affected population. To date, precise pathogenesis of OA has not been fully clarified, which leads to significant obstacles in developing efficacious treatments such as failures in finding disease-modifying OA drugs (DMOADs) in the last decades. Given that diarthrodial joints primarily display the weight-bearing and movement-supporting function, it is not surprising that mechanical stress represents one of the major risk factors for OA. However, the inner connection between mechanical stress and OA onset/progression has yet to be explored. Mitochondrion, a widespread organelle involved in complex biological regulation processes such as adenosine triphosphate (ATP) synthesis and cellular metabolism, is believed to have a controlling role in the survival and function implement of chondrocytes, the singular cell type within cartilage. Mitochondrial dysfunction has also been observed in osteoarthritic chondrocytes. In this review, we systemically summarize mitochondrial alterations in chondrocytes during OA progression and discuss our recent progress in understanding the potential role of mitochondria in mediating mechanical stress-associated osteoarthritic alterations of chondrocytes. In particular, we propose the potential signaling pathways that may regulate this process, which provide new views and therapeutic targets for the prevention and treatment of mechanical stress-associated OA.

Indexed as

Adenosine TriphosphateAnimalsChondrocytesHumansMitochondriaOsteoarthritisQuality of LifeRisk FactorsSignal TransductionStress, MechanicalAdenosine TriphosphateChondrocyte, MitochondriaMechanical stimuliMechanotransductionMitonuclear communicationOsteoarthritis

Identifiers

PMID33086121
PMCPMC7736591
OpenAlexW3093630779

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.