Evidence map›Paper›PMID 35377804›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

Neutrophil and natural killer cell imbalances prevent muscle stem cell-mediated regeneration following murine volumetric muscle loss.

Jacqueline A Larouche, Paula M Fraczek, Sarah J Kurpiers, Benjamin A Yang, Carol Davis, Jesus A Castor-Macias, Kaitlyn Sabin, Shannon Anderson, Julia Harrer, Matthew Hall and 5 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  3. Unconventional functions of natural killer cells in homeostasis and disease.Journal of immunology (Baltimore, Md. : 1950) · 2026
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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

15 authors at 3 institutions in 1 country.

Jacqueline A LaroucheDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0001-9380-3547
Paula M FraczekDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0002-9897-0720
Sarah J KurpiersDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.
Benjamin A YangDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0001-7412-6261
Carol DavisDepartment of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0003-3082-8995
Jesus A Castor-MaciasDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0002-2501-1035
Kaitlyn SabinDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.
Shannon AndersonDepartment of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA 30332.
Julia HarrerDepartment of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA 30332.ORCID 0000-0003-0878-8659
Matthew HallDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.
Susan V BrooksDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0003-1954-967X
Young C JangDepartment of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA 30332.ORCID 0000-0002-9489-2104
Nick WillettPhil and Penny Knight Campus for Accelerating Scientific Impact, University of Oregon, Eugene, OR 97403.
Lonnie D SheaDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.
Carlos A AguilarDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109.ORCID 0000-0003-3830-0634
University of Michigan · USGeorgia Institute of Technology · USUniversity of Oregon · US

Funding

Research Education CoreP30AG024824 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Neil Alexander · 2004 to 2026
$29.2M
Structure, Composition, & Histology Core - Core BP30AR069620 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KARL J JEPSEN · 2016 to 2026
$8.4M
University of Michigan Postbaccalaureate Research Education Program (UM PREP)R25GM086262 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ALLEN, BENJAMIN · 2009 to 2024
$6.1M
NIAMS NIH HHS P30 AR069620NIA NIH HHS P30 AG024824NIGMS NIH HHS R25 GM086262
6 · The paper itself

Abstract

Volumetric muscle loss (VML) overwhelms the innate regenerative capacity of mammalian skeletal muscle (SkM), leading to numerous disabilities and reduced quality of life. Immune cells are critical responders to muscle injury and guide tissue resident stem cell– and progenitor-mediated myogenic repair. However, how immune cell infiltration and intercellular communication networks with muscle stem cells are altered following VML and drive pathological outcomes remains underexplored. Herein, we contrast the cellular and molecular mechanisms of VML injuries that result in the fibrotic degeneration or regeneration of SkM. Following degenerative VML injuries, we observed the heightened infiltration of natural killer (NK) cells as well as the persistence of neutrophils beyond 2 wk postinjury. Functional validation of NK cells revealed an antagonistic role in neutrophil accumulation in part via inducing apoptosis and CCR1-mediated chemotaxis. The persistent infiltration of neutrophils in degenerative VML injuries was found to contribute to impairments in muscle stem cell regenerative function, which was also attenuated by transforming growth factor beta 1 (TGFβ1). Blocking TGFβ signaling reduced neutrophil accumulation and fibrosis and improved muscle-specific force. Collectively, these results enhance our understanding of immune cell–stem cell cross talk that drives regenerative dysfunction and provide further insight into possible avenues for fibrotic therapy exploration.

Indexed as

Killer Cells, NaturalMuscle, SkeletalMuscular DiseasesNeutrophilsRegenerationSatellite Cells, Skeletal MuscleAnimalsFibrosisMiceNeutrophil InfiltrationTransforming Growth Factor betaTransforming Growth Factor betainflammationmuscle stem cellssingle-cell RNA sequencingskeletal muscle

Identifiers

PMID35377804
PMCPMC9169656
OpenAlexW4226053176

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.