Evidence map›Paper›PMID 28978553›Full record

ArticleCirculation2017

C1q/Tumor Necrosis Factor-Related Protein-9 Regulates the Fate of Implanted Mesenchymal Stem Cells and Mobilizes Their Protective Effects Against Ischemic Heart Injury via Multiple Novel Signaling Pathways.

Wenjun Yan, Yongzhen Guo, Ling Tao, Wayne Bond Lau, Lu Gan, Zheyi Yan, Rui Guo, Erhe Gao, G William Wong, Walter L Koch and 2 more

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
12.1field-weighted citation impact, top 1% 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

70 citing papers in PubMed, 137 citations in OpenAlex.

  1. Article
  2. Review
  3. Unveiling the roles of CTRP family in cardiac remodeling.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. The Role of Stem Cells in the Treatment of Cardiovascular Diseases.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Article
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  14. Review
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10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 2 countries.

Wenjun YanDepartment of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA (W.Y., Y.G., W.B.L., L.G., Z.Y., R.G., Y.W., X.-L.M.).
Yongzhen GuoDepartment of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA (W.Y., Y.G., W.B.L., L.G., Z.Y., R.G., Y.W., X.-L.M.).
Ling TaoDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, China (W.Y., L.T.).
Wayne Bond LauDepartment of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA (W.Y., Y.G., W.B.L., L.G., Z.Y., R.G., Y.W., X.-L.M.).
Lu GanDepartment of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA (W.Y., Y.G., W.B.L., L.G., Z.Y., R.G., Y.W., X.-L.M.).
Zheyi YanDepartment of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA (W.Y., Y.G., W.B.L., L.G., Z.Y., R.G., Y.W., X.-L.M.).
Rui GuoDepartment of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA (W.Y., Y.G., W.B.L., L.G., Z.Y., R.G., Y.W., X.-L.M.).
Erhe GaoCenter for Translational Medicine, Temple University, Philadelphia, PA (E.G., W.L.K.).
G William WongDepartment of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD (G.W.W.).
Walter L KochCenter for Translational Medicine, Temple University, Philadelphia, PA (E.G., W.L.K.).
Yajing WangDepartment of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA (W.Y., Y.G., W.B.L., L.G., Z.Y., R.G., Y.W., X.-L.M.).
Xin-Liang MaDepartment of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA (W.Y., Y.G., W.B.L., L.G., Z.Y., R.G., Y.W., X.-L.M.). xin.ma@jefferson.edu yajing.wang@jefferson.edu.
Thomas Jefferson University · USTemple University · USAir Force Medical University · CNJohns Hopkins University · USXijing Hospital · CN

Funding

CTRP and Metabolic ControlR01DK084171 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI Guang William Wong · 2010 to 2026
$8.0M
Targeting Adiponectin for Cardioprotection in the Ischemic HeartR01HL096686 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI MA, XIN-LIANG, WANG, YAJING · 2010 to 2024
$4.7M
Cav-3 in Diabetic Myocardial Injury Following Ischemia/ReperfusionR01HL123404 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI MA, XIN-LIANG · 2015 to 2023
$2.7M
Vevo 2100 ultrasound scannerS10OD010408 · OD · THOMAS JEFFERSON UNIVERSITY · PI FORSBERG, FLEMMING · 2012 to 2012
$525k
Cav-3 in Diabetic Myocardial Injury Following Ischemia/ReperfusionR56HL123404 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI MA, XIN-LIANG · 2014 to 2014
$388k
NHLBI NIH HHS R01 HL096686NHLBI NIH HHS R01 HL123404NHLBI NIH HHS R56 HL123404NIDDK NIH HHS R01 DK084171NIH HHS S10 OD010408
6 · The paper itself

Abstract

backgroundCell therapy remains the most promising approach against ischemic heart injury. However, the poor survival of engrafted stem cells in the ischemic environment limits their therapeutic efficacy for cardiac repair after myocardial infarction. CTRP9 (C1q/tumor necrosis factor-related protein-9) is a novel prosurvival cardiokine with significantly downregulated expression after myocardial infarction. Here we tested a hypothesis that CTRP9 might be a cardiokine required for a healthy microenvironment promoting implanted stem cell survival and cardioprotection.

methodsMice were subjected to myocardial infarction and treated with adipose-derived mesenchymal stem cells (ADSCs, intramyocardial transplantation), CTRP9, or their combination. Survival, cardiac remodeling and function, cardiomyocytes apoptosis, and ADSCs engraftment were evaluated. Whether CTRP9 directly regulates ADSCs function was determined in vitro. Discovery-drive approaches followed by cause-effect analysis were used to uncover the molecular mechanisms of CTRP9.

resultsAdministration of ADSCs alone failed to exert significant cardioprotection. However, administration of ADSCs in addition to CTRP9 further enhanced the cardioprotective effect of CTRP9 (

conclusionsWe provide the first evidence that CTRP9 promotes ADSCs proliferation/survival, stimulates ADSCs migration, and attenuates cardiomyocyte cell death by previously unrecognized signaling mechanisms. These include binding with N-cadherin, activation of ERK-matrix metallopeptidase 9 and ERK-nuclear factor erythroid-derived 2-like 2 signaling, and upregulation/secretion of antioxidative proteins. These results suggest that CTRP9 is a cardiokine critical in maintaining a healthy microenvironment facilitating stem cell engraftment in infarcted myocardial tissue, thereby enhancing stem cell therapeutic efficacy.

Indexed as

RegenerationSignal TransductionAdiponectinAdipose TissueAnimalsApoptosisCadherinsCell MovementCell ProliferationCells, CulturedDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesFibrosisGlycoproteinsGreen Fluorescent ProteinsHydrogen PeroxideAdiponectinCadherinsCdh2 protein, mouseCTRP9 protein, mouseenhanced green fluorescent proteinExtracellular Signal-Regulated MAP KinasesGlycoproteinsGreen Fluorescent ProteinsHydrogen PeroxideMatrix Metalloproteinase 9Mmp9 protein, mouseNfe2l2 protein, mouseNF-E2-Related Factor 2Sod3 protein, mouseSuperoxide Dismutasecardiokinesischemic heart injuryN-cadherinstem cell

Identifiers

PMID28978553
PMCPMC5705403
OpenAlexW2763827226

What OpenQuestion holds

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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.