Evidence map›Paper›PMID 32048631›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2020

Deficiency of Interleukin-36 Receptor Protected Cardiomyocytes from Ischemia-Reperfusion Injury in Cardiopulmonary Bypass.

Cheng Luo, Xiaoyong Xie, Xu Feng, Binfeng Lei, Chen Fang, Yugui Li, Xiongwei Cai, Guoxing Ling, Baoshi Zheng

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

Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Cheng LuoThe First Affiliated Hospital of Guangxi Medical University, Cardiac Surgery Ward, Nanning, Guangxi, China (mainland).
Xiaoyong XieThe First Affiliated Hospital of Guangxi Medical University, Cardiac Surgery Ward, Nanning, Guangxi, China (mainland).
Xu FengThe First Affiliated Hospital of Guangxi Medical University, Cardiac Surgery Ward, Nanning, Guangxi, China (mainland).
Binfeng LeiThe First Affiliated Hospital of Guangxi Medical University, Cardiac Surgery Ward, Nanning, Guangxi, China (mainland).
Chen FangThe First Affiliated Hospital of Guangxi Medical University, Cardiac Surgery Ward, Nanning, Guangxi, China (mainland).
Yugui LiThe First Affiliated Hospital of Guangxi Medical University, Cardiac Surgery Ward, Nanning, Guangxi, China (mainland).
Xiongwei CaiThe First Affiliated Hospital of Guangxi Medical University, Cardiac Surgery Ward, Nanning, Guangxi, China (mainland).
Guoxing LingThe First Affiliated Hospital of Guangxi Medical University, Cardiac Surgery Ward, Nanning, Guangxi, China (mainland).
Baoshi ZhengThe First Affiliated Hospital of Guangxi Medical University, Cardiac Surgery Ward, Nanning, Guangxi, China (mainland).
First Affiliated Hospital of GuangXi Medical University · CNGuangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Interleukin-36 has been demonstrated to be involved in inflammatory responses. Inflammatory responses due to ischemia-reperfusion injury following cardiopulmonary bypass (CPB) can cause heart dysfunction or damage. MATERIAL AND METHODS The CPB models were constructed in IL-36R-/-, IL-36RN-/-, and wild-type SD rats. Ultrasonic cardiography and ELISA were used to evaluate the cardiac function and measuring myocardial biomarker levels in different groups. TUNEL assay was used to evaluate apoptosis. Western blot assays and RT-PCR were performed to measure the expression of chemokines and secondary inflammatory cytokines in the heart. Oxidative stress in tissue and cultured cells was assessed using a DCFH-DA fluorescence probe and quantification of superoxide dismutase activity. RESULTS Improved systolic function and decreased serum levels of myocardial damage biomarkers were found in IL-36R-/- rats compared to WT rats, while worse cardiac function and cardiomyocyte IR injury were observed in IL-36RN-/- rats compared to WT rats. TUNEL staining and Western blot analyses found that cardiomyocyte apoptosis and inflammation were significantly lower in the hearts of IL-36R-/- rats compared with that of WT rats. Oxidative stress was significantly lower in IL-36R-/- rats compared to WT rats. iNOS expression was significantly reduced, while eNOS expression was increased in the hearts of IL-36R-/- rats. Silencing of IL-36R expression in vitro activated SIRT1/FOXO1/p53 signaling in cardiomyocytes. CONCLUSIONS IL-36R deficiency in cardiomyocytes repressed infiltration of bone marrow-derived inflammatory cells and oxidative stress dependent on SIRT1-FOXO1 signaling, thus protecting cardiomyocytes and improving cardiac function in CPB model rats.

Indexed as

AnimalsCardiopulmonary BypassDisease Models, AnimalForkhead Box Protein O1Gene Knockout TechniquesHumansMaleMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacNerve Tissue ProteinsOxidative StressRatsRats, TransgenicReceptors, InterleukinSignal TransductionForkhead Box Protein O1Foxo1 protein, ratIl1rl2 protein, ratNerve Tissue ProteinsReceptors, InterleukinSirt1 protein, ratSirtuin 1

Identifiers

PMID32048631
PMCPMC7034403
OpenAlexW3002400405

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.