Evidence map›Paper›PMID 32820177›Full record

ArticleNature communications2020

Inhibition of inflammatory CCR2 signaling promotes aged muscle regeneration and strength recovery after injury.

Roméo S Blanc, Jacob G Kallenbach, John F Bachman, Amanda Mitchell, Nicole D Paris, Joe V Chakkalakal

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 8% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Roméo S BlancDepartment of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY, USA.ORCID http://orcid.org/0000-0001-7069-4085
Jacob G KallenbachDepartment of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY, USA.ORCID http://orcid.org/0000-0002-0405-1521
John F BachmanDepartment of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY, USA.
Amanda MitchellDepartment of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY, USA.
Nicole D ParisDepartment of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY, USA.
Joe V ChakkalakalDepartment of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY, USA. joe_chakkalakal@urmc.rochester.edu.ORCID http://orcid.org/0000-0002-8440-7312
University of Rochester Medical Center · US

Funding

The University of Rochester Core Center for Musculoskeletal Biology and MedicineP30AR061307 · NIAMS · UNIVERSITY OF ROCHESTER · PI SCHWARZ, EDWARD M. · 2011 to 2015
$3.0M
Interrelationships between age-related skeletal muscle stem cell and NMJ declineR01AG051456 · NIA · UNIVERSITY OF ROCHESTER · PI CHAKKALAKAL, JOE · 2015 to 2019
$1.9M
Cellular Basis for Radiation induced acceleration of sarcopenia in juvenile cancer survivorsR01CA220467 · NCI · UNIVERSITY OF ROCHESTER · PI CHAKKALAKAL, JOE · 2017 to 2021
$1.8M
NCI NIH HHS R01 CA220467NIAMS NIH HHS P30 AR061307NIA NIH HHS R01 AG051456
6 · The paper itself

Abstract

Muscle regeneration depends on a robust albeit transient inflammatory response. Persistent inflammation is a feature of age-related regenerative deficits, yet the underlying mechanisms are poorly understood. Here, we find inflammatory-related CC-chemokine-receptor 2 (Ccr2) expression in non-hematopoietic myogenic progenitors (MPs) during regeneration. After injury, the expression of Ccr2 in MPs corresponds to the levels of its ligands, the chemokines Ccl2, 7, and 8. We find stimulation of Ccr2-activity inhibits MP fusion and contribution to myofibers. This occurs in association with increases in MAPKp38δ/γ signaling, MyoD phosphorylation, and repression of the terminal myogenic commitment factor Myogenin. High levels of Ccr2-chemokines are a feature of regenerating aged muscle. Correspondingly, deletion of Ccr2 in MPs is necessary for proper fusion into regenerating aged muscle. Finally, opportune Ccr2 inhibition after injury enhances aged regeneration and functional recovery. These results demonstrate that inflammatory-induced activation of Ccr2 signaling in myogenic cells contributes to aged muscle regenerative decline.

Indexed as

Age FactorsAnimalsCell TransplantationChemokine CCL2Chemokine CCL7Chemokine CCL8Inflammation MediatorsMice, Inbred C57BLMice, KnockoutMuscle DevelopmentMuscle, SkeletalMyogeninReceptors, CCR2RegenerationSatellite Cells, Skeletal MuscleSignal TransductionChemokine CCL2Chemokine CCL7Chemokine CCL8Inflammation MediatorsMyogeninReceptors, CCR2

Identifiers

PMID32820177
PMCPMC7441393
OpenAlexW3065548143

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.