Evidence map›Paper›PMID 21145579›Full record

ArticleCell2010

Short telomeres and stem cell exhaustion model Duchenne muscular dystrophy in mdx/mTR mice.

Alessandra Sacco, Foteini Mourkioti, Rose Tran, Jinkuk Choi, Michael Llewellyn, Peggy Kraft, Marina Shkreli, Scott Delp, Jason H Pomerantz, Steven E Artandi and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 306 papers.

0numbers the graph read from it
0cells of the map it votes in
306citing papers in PubMed
13.1field-weighted citation impact, top 1% 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

306 citing papers in PubMed, 504 citations in OpenAlex.

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  19. FAPs orchestrate homeostasis of muscle physiology and pathophysiology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Review
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246 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Alessandra SaccoBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
Foteini Mourkioti
Rose Tran
Jinkuk Choi
Michael Llewellyn
Peggy Kraft
Marina Shkreli
Scott Delp
Jason H Pomerantz
Steven E Artandi
Helen M Blau
Stanford University · US

Funding

Basic and Translational Research iPSC-based hematologic and vascular therapiesU01HL100397 · NHLBI · STANFORD UNIVERSITY · PI COOKE, JOHN P · 2009 to 2015
$7.4M
Stem Cells for Brain and BrawnR01AG020961 · NIA · STANFORD UNIVERSITY · PI BLAU, HELEN M · 2002 to 2019
$5.0M
ACTIVATORS OF MUSCLE GENESR01AG009521 · NIA · STANFORD UNIVERSITY · PI BLAU, HELEN M · 1990 to 2014
$4.7M
Regulation of Hematopoietic Stem Cell Fate in Bioengineered NichesR01HL096113 · NHLBI · STANFORD UNIVERSITY · PI BLAU, HELEN M · 2009 to 2013
$2.7M
ACTIVATORS OF HUMAN MUSCLE GENESR37AG009521 · NIA · STANFORD UNIVERSITY · PI BLAU, HELEN M · 1995 to 2004
$2.3M
NHLBI NIH HHS R01 HL096113NHLBI NIH HHS U01 HL100397NIA NIH HHS AG009521NIA NIH HHS AG020961NIA NIH HHS R01 AG009521NIA NIH HHS R01 AG020961NIA NIH HHS R37 AG009521
6 · The paper itself

Abstract

In Duchenne muscular dystrophy (DMD), dystrophin mutation leads to progressive lethal skeletal muscle degeneration. For unknown reasons, dystrophin deficiency does not recapitulate DMD in mice (mdx), which have mild skeletal muscle defects and potent regenerative capacity. We postulated that human DMD progression is a consequence of loss of functional muscle stem cells (MuSC), and the mild mouse mdx phenotype results from greater MuSC reserve fueled by longer telomeres. We report that mdx mice lacking the RNA component of telomerase (mdx/mTR) have shortened telomeres in muscle cells and severe muscular dystrophy that progressively worsens with age. Muscle wasting severity parallels a decline in MuSC regenerative capacity and is ameliorated histologically by transplantation of wild-type MuSC. These data show that DMD progression results, in part, from a cell-autonomous failure of MuSC to maintain the damage-repair cycle initiated by dystrophin deficiency. The essential role of MuSC function has therapeutic implications for DMD.

Indexed as

Disease Models, AnimalMiceAnimalsCell ProliferationDystrophinHumansMice, Inbred mdxMuscular Dystrophy, AnimalMuscular Dystrophy, DuchennePrejudiceStem CellsTelomereDystrophin

Identifiers

PMID21145579
PMCPMC3025608
OpenAlexW2157735441

What OpenQuestion holds

Textmetadata
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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.