Evidence map›Paper›PMID 36409464›Full record

ArticleDiabetes & vascular disease research

C1q/TNF-related protein-2 improved angiogenesis to protect myocardial function during ischaemia‒reperfusion.

Mingfang Ye, Qi-Hong Wu, Ke Yang, Yukun Luo

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Diabetes & vascular disease research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Unveiling the roles of CTRP family in cardiac remodeling.Journal of molecular medicine (Berlin, Germany) · 2025
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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

4 authors at 2 institutions in 1 country.

Mingfang YeDepartment of Cardiology, 117890Fujian Medical University Union Hospital, Fujian Medical Center for Cardiovascular Diseases, Fujian Institute of Coronary Heart Disease, Fujian Key Laboratory of Vascular Aging, Fujian Medical University, Fujian, China.ORCID 0000-0001-6683-1016
Qi-Hong WuDepartment of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, 66281Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-8625-0777
Ke YangDepartment of Cardiovascular Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yukun LuoDepartment of Cardiology, 117890Fujian Medical University Union Hospital, Fujian Medical Center for Cardiovascular Diseases, Fujian Institute of Coronary Heart Disease, Fujian Key Laboratory of Vascular Aging, Fujian Medical University, Fujian, China.
Fujian Medical University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCollateral growth plays an important role in the recovery of acute myocardial infarction. C1q/TNF-related protein-2 (CTRP2), a CTRP family member, showed some protective effects on cell survival. In this study, the relationship between CTRP2 and collateral growth was examined.

methodsC57BL/6 mice were subjected to myocardial ischaemia/reperfusion (I/R), and the expression of CTRP2 and the effect of CTRP2 on infarction size, cardiac function and angiogenesis were examined. The ischaemic hindlimb model was also used to examine the effect of CTRP2. In vitro, CTRP2-mediated regulation of angiogenesis, AKT activation and VEGFR2 expression in endothelial cells was examined. The CTRP2 level associated with good collateral growth was observed in a cohort.

resultsI/R reduced CTRP2 expression, and intraperitoneal injection of recombinant CTRP2 protein improved infarction size, cardiac function and angiogenesis. Overexpression of CTRP2 promoted blood refusion and collateral growth in ischaemic hindlimb mice. In vitro, CTRP2 enhanced tube formation and migration in a dose-dependent manner, while CTRP2 increased AKT phosphorylation and VEGFR2 expression. In an observational clinical cohort, CTRP2 levels were significantly increased in patients with good collateral growth, and CTRP2 was negatively associated with poor collateral growth in patients.

conclusionCTRP2 improved cardiac function by promoting collateral growth by promoting AKT-VEGFR2.

Indexed as

Complement C1qMyocardial InfarctionAnimalsComplement System ProteinsEndothelial CellsIschemiaMiceMice, Inbred C57BLNeovascularization, PathologicProto-Oncogene Proteins c-aktReperfusionComplement C1qComplement System ProteinsCTRP2 protein, mouseProto-Oncogene Proteins c-aktangiogenesiscollateral growthCTRP2myocardial ischaemia/reperfusion

Identifiers

PMID36409464
PMCPMC9706074
OpenAlexW4309658335

What OpenQuestion holds

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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.