Evidence map›Paper›PMID 33361519›Full record

ArticleAging2020

Aberrant RhoA activation in macrophages increases senescence-associated secretory phenotypes and ectopic calcification in muscular dystrophic mice.

Xiaodong Mu, Chi-Yi Lin, William S Hambright, Ying Tang, Sudheer Ravuri, Aiping Lu, Polina Matre, Wanqun Chen, Xueqin Gao, Yan Cui and 3 more

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. The Role of MicroRNA in the Pathogenesis of Duchenne Muscular Dystrophy.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Article
  6. Article
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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

13 authors at 3 institutions in 2 countries.

Xiaodong MuShandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Chi-Yi LinDepartment of Orthopedic Surgery, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
William S HambrightSteadman Philippon Research Institute, Center for Regenerative Sports Medicine, Vail, CO 81657, USA.
Ying TangDepartment of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA 15260, USA.
Sudheer RavuriSteadman Philippon Research Institute, Center for Regenerative Sports Medicine, Vail, CO 81657, USA.
Aiping LuSteadman Philippon Research Institute, Center for Regenerative Sports Medicine, Vail, CO 81657, USA.
Polina MatreDepartment of Orthopedic Surgery, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Wanqun ChenDepartment of Orthopedic Surgery, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Xueqin GaoSteadman Philippon Research Institute, Center for Regenerative Sports Medicine, Vail, CO 81657, USA.
Yan CuiDepartment of Orthopedic Surgery, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Ling ZhongDepartment of Orthopedic Surgery, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Bing WangDepartment of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA 15260, USA.
Johnny HuardSteadman Philippon Research Institute, Center for Regenerative Sports Medicine, Vail, CO 81657, USA.
Steadman Philippon Research Institute · USThe University of Texas Health Science Center at Houston · USUniversity of Pittsburgh · US

Funding

PROTEOMICSP01AG043376 · NIA · UNIVERSITY OF MINNESOTA · PI ROBBINS, PAUL D. · 2013 to 2019
$11.2M
Bone Abnormalities & Healing Defect in Muscular DystrophyR01AR065445 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI HUARD, JOHNNY · 2014 to 2018
$1.7M
NIAMS NIH HHS R01 AR065445NIA NIH HHS P01 AG043376
6 · The paper itself

Abstract

Duchenne Muscular Dystrophy (DMD) patients often suffer from both muscle wasting and osteoporosis. Our previous studies have revealed reduced regeneration potential in skeletal muscle and bone, concomitant with ectopic calcification of soft tissues in double knockout (

Indexed as

AnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticCalcinosisCD68 MoleculeCellular SenescenceDisease Models, AnimalDystrophinMacrophagesMiceMice, KnockoutMuscle, SkeletalMuscular Dystrophy, AnimalMuscular Dystrophy, DuchenneMyocardiumrhoA GTP-Binding ProteinAntigens, CDAntigens, Differentiation, MyelomonocyticCD68 MoleculeCD68 protein, mouseDystrophinrhoA GTP-Binding ProteinRhoA protein, mouserho-Associated KinasesUtrophincellular senescencechronic inflammationheterotopic ossificationmuscle dystrophymuscle stem cell

Identifiers

PMID33361519
PMCPMC7803538
OpenAlexW3115865729

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.