Evidence map›Paper›PMID 29233958›Full record

ArticleNature communications2017

Complement C3a signaling facilitates skeletal muscle regeneration by regulating monocyte function and trafficking.

Congcong Zhang, Chunxiao Wang, Yulin Li, Takashi Miwa, Chang Liu, Wei Cui, Wen-Chao Song, Jie Du

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

68 citing papers in PubMed, 118 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Multifunctional scaffold based on TiMaterials today. Bio · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Congcong ZhangBeijing AnZhen Hospital, Capital Medical University, The Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, 100029, China.
Chunxiao WangBeijing AnZhen Hospital, Capital Medical University, The Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, 100029, China.
Yulin LiBeijing AnZhen Hospital, Capital Medical University, The Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, 100029, China.
Takashi MiwaDepartment of Pharmacology and Institute for Translational Medicine and Therapeutics, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA, 19104, USA.
Chang LiuBeijing AnZhen Hospital, Capital Medical University, The Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, 100029, China.
Wei CuiBeijing AnZhen Hospital, Capital Medical University, The Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, 100029, China.
Wen-Chao SongDepartment of Pharmacology and Institute for Translational Medicine and Therapeutics, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA, 19104, USA. songwe@upenn.edu.
Jie DuBeijing AnZhen Hospital, Capital Medical University, The Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, 100029, China. jiedu@ccmu.edu.cn.
Capital Medical University · CNTranslational Therapeutics (United States) · USUniversity of Pennsylvania · US

Funding

BIOLOGY OF DECAY ACCELERATING FACTORR01AI044970 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI SONG, WENCHAO · 2000 to 2014
$4.9M
Pathogenesis and therapy of dense deposit disease in a mouse modelR01AI085596 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI SONG, WENCHAO · 2010 to 2019
$3.5M
NIAID NIH HHS R01 AI044970NIAID NIH HHS R01 AI085596
6 · The paper itself

Abstract

Regeneration of skeletal muscle following injury is accompanied by transient inflammation. Here we show that complement is activated in skeletal muscle injury and plays a key role during regeneration. Genetic ablation of complement C3 or its inactivation with Cobra Venom Factor (CVF) result in impaired muscle regeneration following cardiotoxin-induced injury in mice. The effect of complement in muscle regeneration is mediated by the alternative pathway and C3a receptor (C3aR) signaling, as deletion of Cfb, a key alternative pathway component, or C3aR leads to impaired regeneration and reduced monocyte/macrophage infiltration. Monocytes from C3aR-deficient mice express a reduced level of adhesion molecules, cytokines and genes associated with antigen processing and presentation. Exogenous administration of recombinant CCL5 to C3aR-deficient mice rescues the defects in inflammatory cell recruitment and regeneration. These findings reveal an important role of complement C3a in skeletal muscle regeneration, and suggest that manipulating complement system may produce therapeutic benefit in muscle injury and regeneration.

Indexed as

AnimalsBone Marrow TransplantationCardiotoxinsCell MovementCells, CulturedChemokine CCL5ChimeraComplement C3aComplement Pathway, AlternativeDisease Models, AnimalElapid VenomsHumansInflammationMacrophagesMaleMiceCardiotoxinsCcl5 protein, mouseChemokine CCL5cobra venom factorComplement C3acomplement C3a receptorElapid VenomsReceptors, Complement

Identifiers

PMID29233958
PMCPMC5727192
OpenAlexW2773549048

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.