Evidence map›Paper›PMID 27277683›Full record

ArticleCell death & disease2016

MicroRNA-155 facilitates skeletal muscle regeneration by balancing pro- and anti-inflammatory macrophages.

M Nie, J Liu, Q Yang, H Y Seok, X Hu, Z-L Deng, D-Z Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

41 citing papers in PubMed, 68 citations in OpenAlex.

  1. Regenerative Medicine: Advanced Therapy for Muscle Tissue Restoration.International journal of molecular sciences · 2026
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  10. Investigating the Causal Effects of Exercise-Induced Genes on Sarcopenia.International journal of molecular sciences · 2024
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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

7 authors at 4 institutions in 2 countries.

M NieDepartment of Orthopaedic Surgery, The Second Affiliated Hospital, Chongqing Medical University, 76 Linjiang Road, Chongqing, P.R. China.
J LiuDepartment of Cardiology, Boston Children's Hospital, Harvard Medical School, 320 Longwood Avenue, Boston, MA, USA.
Q YangDepartment of Cardiology, Boston Children's Hospital, Harvard Medical School, 320 Longwood Avenue, Boston, MA, USA.
H Y SeokDepartment of Cardiology, Boston Children's Hospital, Harvard Medical School, 320 Longwood Avenue, Boston, MA, USA.
X HuDepartment of Cardiology, Boston Children's Hospital, Harvard Medical School, 320 Longwood Avenue, Boston, MA, USA.
Z-L DengDepartment of Orthopaedic Surgery, The Second Affiliated Hospital, Chongqing Medical University, 76 Linjiang Road, Chongqing, P.R. China.
D-Z WangDepartment of Cardiology, Boston Children's Hospital, Harvard Medical School, 320 Longwood Avenue, Boston, MA, USA.
Boston Children's Hospital · USDalian Medical University · CNHarvard University · USSichuan Agricultural University · CN

Funding

RESEARCH METHODS IN PEDIATRICS HEART DISEASET32HL007572 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI Sarah D DE FERRANTI, Jane W. Newburger · 1985 to 2026
$13.0M
MicroRNAs, cardiac development and functionR01HL085635 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WANG, DA-ZHI · 2007 to 2015
$3.2M
Molecular Mechanisms of Dilated CardiomyopathyR01HL116919 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI WANG, DA-ZHI · 2013 to 2016
$1.7M
NHLBI NIH HHS R01 HL085635NHLBI NIH HHS R01 HL116919NHLBI NIH HHS T32 HL007572
6 · The paper itself

Abstract

Skeletal muscle has remarkable regeneration capacity and regenerates in response to injury. Muscle regeneration largely relies on muscle stem cells called satellite cells. Satellite cells normally remain quiescent, but in response to injury or exercise they become activated and proliferate, migrate, differentiate, and fuse to form multinucleate myofibers. Interestingly, the inflammatory process following injury and the activation of the myogenic program are highly coordinated, with myeloid cells having a central role in modulating satellite cell activation and regeneration. Here, we show that genetic deletion of microRNA-155 (miR-155) in mice substantially delays muscle regeneration. Surprisingly, miR-155 does not appear to directly regulate the proliferation or differentiation of satellite cells. Instead, miR-155 is highly expressed in myeloid cells, is essential for appropriate activation of myeloid cells, and regulates the balance between pro-inflammatory M1 macrophages and anti-inflammatory M2 macrophages during skeletal muscle regeneration. Mechanistically, we found that miR-155 suppresses SOCS1, a negative regulator of the JAK-STAT signaling pathway, during the initial inflammatory response upon muscle injury. Our findings thus reveal a novel role of miR-155 in regulating initial immune responses during muscle regeneration and provide a novel miRNA target for improving muscle regeneration in degenerative muscle diseases.

Indexed as

RegenerationAnimalsCell DifferentiationCytokinesInflammationJanus KinasesMacrophagesMice, Inbred C57BLMice, KnockoutMicroRNAsModels, BiologicalMuscle, SkeletalMyoblastsPhenotypeSatellite Cells, Skeletal MuscleSTAT Transcription FactorsCytokinesJanus KinasesMicroRNAsMirn155 microRNA, mouseSocs1 protein, mouseSTAT Transcription FactorsSuppressor of Cytokine Signaling 1 Protein

Identifiers

PMID27277683
PMCPMC5143393
OpenAlexW2418551143

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.