Evidence map›Paper›PMID 37502924›Full record

ArticlebioRxiv : the preprint server for biology2023

Identification of Periostin as a critical niche for myofibroblast dynamics and fibrosis during tendon healing.

Jessica E Ackerman, Emmanuela Adjei-Sowah, Antonion Korcari, Samantha N Muscat, Anne E C Nichols, Mark R Buckley, Alayna E Loiselle

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

Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed, 4 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 2 countries.

Jessica E AckermanCenter for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.
Emmanuela Adjei-SowahCenter for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.
Antonion KorcariCenter for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.
Samantha N MuscatCenter for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.
Anne E C NicholsCenter for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.
Mark R BuckleyCenter for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.
Alayna E LoiselleCenter for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.
University of Rochester Medical Center · US

Funding

Rochester Resource-Based Center for Bone, Muscle and Orthopaedic Research (ROCSTARR) (Overall Application)P30AR069655 · NIAMS · UNIVERSITY OF ROCHESTER · PI Edward M. Schwarz · 2016 to 2026
$7.8M
Modulating Cell-fate to Promote Regenerative Tendon HealingR01AR077527 · NIAMS · UNIVERSITY OF ROCHESTER · PI LOISELLE, ALAYNA · 2021 to 2025
$2.0M
s100a4 Signaling in Fibrotic Diabetic Tendon HealingR01AR073169 · NIAMS · UNIVERSITY OF ROCHESTER · PI LOISELLE, ALAYNA · 2018 to 2022
$1.7M
Epitenon-derived progenitor cells in tendon healing and adaptationR00AR080757 · NIAMS · UNIVERSITY OF ROCHESTER · PI Anne E.C. Nichols · 2024 to 2026
$727k
Epitenon-derived progenitor cells in tendon healing and adaptationK99AR080757 · NIAMS · UNIVERSITY OF ROCHESTER · PI NICHOLS, ANNE E.C. · 2022 to 2023
$283k
Myofibroblast mediated mechanisms of fibrotic tendon healingF31AR077398 · NIAMS · UNIVERSITY OF ROCHESTER · PI ACKERMAN, JESSICA EVE · 2020 to 2021
$92k
NIAMS NIH HHS F31 AR077398NIAMS NIH HHS K99 AR080757NIAMS NIH HHS P30 AR069655NIAMS NIH HHS R00 AR080757NIAMS NIH HHS R01 AR073169NIAMS NIH HHS R01 AR077527
6 · The paper itself

Abstract

Tendon injuries are a major clinical problem, with poor patient outcomes caused by abundant scar tissue deposition during healing. Myofibroblasts play a critical role in the initial restoration of structural integrity after injury. However, persistent myofibroblast activity drives the transition to fibrotic scar tissue formation. As such, disrupting myofibroblast persistence is a key therapeutic target. While myofibroblasts are typically defined by the presence of αSMA+ stress fibers, αSMA is expressed in other cell types including the vasculature. As such, modulation of myofibroblast dynamics via disruption of αSMA expression is not a translationally tenable approach. Recent work has demonstrated that Periostin-lineage (Postn

Indexed as

extracellular matrixPeriostinscar tissuetendon

Identifiers

PMID37502924
PMCPMC10370208
OpenAlexW4385145574

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.