Evidence map›Paper›PMID 21689628›Full record

ArticleThe American journal of pathology2011

Follistatin improves skeletal muscle healing after injury and disease through an interaction with muscle regeneration, angiogenesis, and fibrosis.

Jinhong Zhu, Yong Li, Aiping Lu, Burhan Gharaibeh, Jianqun Ma, Tetsuo Kobayashi, Andres J Quintero, Johnny Huard

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
4.3field-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

70 citing papers in PubMed, 117 citations in OpenAlex.

  1. Trial
  2. A phase 1/2a follistatin gene therapy trial for becker muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2015
    Trial
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10 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 3 countries.

Jinhong ZhuStem Cell Research Center, University of Pittsburgh, Pittsburgh, Pennsylvania 15219, USA.
Yong Li
Aiping Lu
Burhan Gharaibeh
Jianqun Ma
Tetsuo Kobayashi
Andres J Quintero
Johnny Huard
University of Pittsburgh · USHarbin Medical University · CN

Funding

IMPROVING MUSCLE HEALING THROUGH PREVENTION OF FIBROSISR01AR047973 · NIAMS · CHILDREN'S HOSP PITTSBURGH/UPMC HLTH SYS · PI HUARD, JOHNNY · 2001 to 2004
$1.1M
NIAMS NIH HHS R01 AR047973NIAMS NIH HHS R01 AR47973
6 · The paper itself

Abstract

Recovery from skeletal muscle injury is often incomplete because of the formation of fibrosis and inadequate myofiber regeneration; therefore, injured muscle could benefit significantly from therapies that both stimulate muscle regeneration and inhibit fibrosis. To this end, we focused on blocking myostatin, a member of the transforming growth factor-β superfamily and a negative regulator of muscle regeneration, with the myostatin antagonist follistatin. In vivo, follistatin-overexpressing transgenic mice underwent significantly greater myofiber regeneration and had less fibrosis formation compared with wild-type mice after skeletal muscle injury. Follistatin's mode of action is likely due to its ability to block myostatin and enhance neovacularization. Furthermore, muscle progenitor cells isolated from follistatin-overexpressing mice were significantly superior to muscle progenitors isolated from wild-type mice at regenerating dystrophin-positive myofibers when transplanted into the skeletal muscle of dystrophic mdx/severe combined immunodeficiency mice. In vitro, follistatin stimulated myoblasts to express MyoD, Myf5, and myogenin, which are myogenic transcription factors that promote myogenic differentiation. Moreover, follistatin's ability to enhance muscle differentiation is at least partially due to its ability to block myostatin, activin A, and transforming growth factor-β1, all of which are negative regulators of muscle cell differentiation. The findings of this study suggest that follistatin is a promising agent for improving skeletal muscle healing after injury and muscle diseases, such as the muscular dystrophies.

Indexed as

AnimalsCell LineCell TransplantationFibrosisFollistatinMaleMiceMice, Inbred C57BLMice, KnockoutMicroscopy, FluorescenceMuscle, SkeletalMyoD ProteinMyogenic Regulatory Factor 5MyostatinNeovascularization, PathologicRegenerationFollistatinMyf5 protein, mouseMyoD ProteinMyogenic Regulatory Factor 5MyostatinTransforming Growth Factor beta

Identifiers

PMID21689628
PMCPMC3157209
OpenAlexW2148324418

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.