Evidence map›Paper›PMID 19893053›Full record

ArticleThe American journal of pathology2009

Chemokine CXCL16 regulates neutrophil and macrophage infiltration into injured muscle, promoting muscle regeneration.

Liping Zhang, Limei Ran, Gabriela E Garcia, Xiaonan H Wang, Shuhua Han, Jie Du, William E Mitch

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

63 citing papers in PubMed, 98 citations in OpenAlex.

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  18. Mechanisms Regulating Muscle Protein Synthesis in CKD.Journal of the American Society of Nephrology : JASN · 2020
    Article
  19. Article
  20. A Critical Role of Formyl Peptide Receptors in Host Defense againstJournal of immunology (Baltimore, Md. : 1950) · 2020
    Article

3 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Liping ZhangNephrology Division, Baylor College of Medicine, Houston, Texas 77030, USA.
Limei Ran
Gabriela E Garcia
Xiaonan H Wang
Shuhua Han
Jie Du
William E Mitch
Baylor College of Medicine · USEmory University · US

Funding

Renal Inflammation: Mechanisms and ConsequencesP50DK064233 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2003 to 2007
$5.1M
PROTEIN NUTRITION IN EXPERIMENTAL UREMIAR37DK037175 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2006 to 2015
$3.8M
CXCL16/CXCR6 and Their Roles in Autoimmune ArthritisR01AI055554 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI HAN, SHUHUA · 2005 to 2010
$1.4M
SMAD SIGNALING IN ANGIOTENSIN II-MEDIATED RENAL FIBROSISR01DK062828 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2005 to 2006
$680k
CXCL 16/CXCR6 and Their Roles in Autoimmune ArthritisR21AI055554 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI HAN, SHUHUA · 2004 to 2004
$301k
NIAID NIH HHS AI055554NIAID NIH HHS R01 AI055554NIAID NIH HHS R21 AI055554NIDDK NIH HHS P50 DK064233NIDDK NIH HHS P50 DK64233NIDDK NIH HHS R01 DK062828NIDDK NIH HHS R01 DK62828NIDDK NIH HHS R37 DK037175NIDDK NIH HHS R37 DK37175
6 · The paper itself

Abstract

Only a few specific chemokines that mediate interactions between inflammatory and satellite cells in muscle regeneration have been identified. The chemokine CXCL16 differs from other chemokines because it has both a transmembrane region and active, soluble chemokine forms. Indeed, we found increased expression of CXCL16 and its receptor, CXCR6, in regenerating myofibers. Muscle regeneration in CXCL16-deficient (CXCL16KO) mice was severely impaired compared with regeneration in wild-type mice. In addition, there was decreased MyoD and myogenin expression in regenerating muscle in CXCL16KO mice, indicating impaired satellite cell proliferation and differentiation. After 1 month, new myofibers in CXCL16KO mice remained significantly smaller than those in muscle of wild-type mice. To understand how CXCL16 regulates muscle regeneration, we examined cells infiltrating injured muscle. There were more infiltrating neutrophils and fewer macrophages in injured muscle of CXCL16KO mice compared with events in wild-type mice. Moreover, absence of CXCL16 led to different expression of cytokines/chemokines in injured muscles: mRNAs of macrophage-inflammatory protein (MIP)-1alpha, MIP-1beta, and MIP-2 were increased, whereas regulated on activation normal T cell expressed and secreted, T-cell activation-3, and monocyte chemoattractant protein-1 mRNAs were lower compared with results in muscles of wild-type mice. Impaired muscle regeneration in CXCL16KO mice also resulted in fibrosis, which was linked to transforming growth factor-beta1 expression. Thus, CXCL16 expression is a critical mediator of muscle regeneration, and it suppresses the development of fibrosis.

Indexed as

AnimalsChemokine CXCL16Chemokine CXCL6ChemokinesImmunohistochemistryMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, SkeletalNeutrophil InfiltrationRegenerationReverse Transcriptase Polymerase Chain ReactionSatellite Cells, Skeletal MuscleChemokine CXCL16Chemokine CXCL6ChemokinesCxcl16 protein, mouse

Identifiers

PMID19893053
PMCPMC2789607
OpenAlexW1979387940

What OpenQuestion holds

Textmetadata
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.