Evidence map›Paper›PMID 27130635›Full record

ReviewSeminars in cell & developmental biology2017

Enhanced cartilage repair in 'healer' mice-New leads in the search for better clinical options for cartilage repair.

Jamie Fitzgerald

Abstract readReview
In one paragraph

Review in Seminars in cell & developmental biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Earlier proteoglycan turnover promotes higher efficiency matrix remodeling in MRL/MpJ tendons.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Hypoxia-inducible factor 1α (HIF-1α) is a major determinant in the enhanced function of muscle-derived progenitors from MRL/MpJ mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    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

1 author.

Jamie FitzgeraldBone and Joint Center, Department of Orthopedic Surgery, Henry Ford Hospital System, Detroit, MI 48202, USA. Electronic address: jfitzge2@hfhs.org.

Funding

Three new collagen VI genes; COL6A4, COL6A5 and COL6A6R01AR055957 · NIAMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI FITZGERALD, JAMIE · 2009 to 2013
$1.5M
NIAMS NIH HHS R01 AR055957
6 · The paper itself

Abstract

Adult articular cartilage has a poor capacity to undergo intrinsic repair. Current strategies for the repair of large cartilage defects are generally unsatisfactory because the restored cartilage does not have the same resistance to biomechanical loading as authentic articular cartilage and degrades over time. Recently, an exciting new research direction, focused on intrinsic cartilage regeneration rather than fibrous repair by external means, has emerged. This review explores the new findings in this rapidly moving field as they relate to the clinical goal of restoration of structurally robust, stable and non-fibrous articular cartilage following injury.

Indexed as

RegenerationAnimalsBiomedical ResearchCartilage, ArticularGenetic Association StudiesMiceWound HealingCartilageEpimorphic regenerationHealer miceMRL/MpJ miceOsteoarthritis

Identifiers

PMID27130635
PMCPMC5269530

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.