Evidence map›Paper›PMID 30782145›Full record

ArticleBMC medicine2019

Cathelicidin-related antimicrobial peptide protects against myocardial ischemia/reperfusion injury.

Yihua Bei, Li-Long Pan, Qiulian Zhou, Cuimei Zhao, Yuan Xie, Chengfei Wu, Xiangmin Meng, Huanyu Gu, Jiahong Xu, Lei Zhou and 5 more

Open access · goldAbstract read
In one paragraph

Article in BMC medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 75 citations in OpenAlex.

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  11. Endopeptidase O promotesVirulence · 2023
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  13. Neutrophil-derived cathelicidin promotes cerebral angiogenesis after ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
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  14. Article
  15. Samarcandin protects against testicular ischemia/reperfusion injury in rats via activation of Nrf2/HO-1-mediated antioxidant responses.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
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  16. Review
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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

15 authors at 10 institutions in 4 countries.

Yihua BeiCardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, 333 Nan Chen Road, Shanghai, 200444, China.
Li-Long PanSchool of Medicine, Jiangnan University, Wuxi, 214122, China.
Qiulian ZhouCardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, 333 Nan Chen Road, Shanghai, 200444, China.
Cuimei ZhaoDepartment of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Yuan XieDepartment of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Chengfei WuState Key Laboratory of Food Science and Technology, Jiangnan University, 1800 Lihu Avenue, Wuxi, 214122, Jiangsu, China.
Xiangmin MengCardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, 333 Nan Chen Road, Shanghai, 200444, China.
Huanyu GuDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Jiahong XuDepartment of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Lei ZhouDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Joost P G SluijterDepartment of Cardiology, Laboratory of Experimental Cardiology, University Utrecht, University Medical Center Utrecht, 3584 CX, Utrecht, The Netherlands.
Saumya DasCardiovascular Division of the Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.
Birgitta AgerberthDepartment of Laboratory Medicine, Division of Clinical Microbiology, Karolinska Institutet, Karolinska University Hospital Huddinge, F68, Stockholm, Sweden.
Jia SunState Key Laboratory of Food Science and Technology, Jiangnan University, 1800 Lihu Avenue, Wuxi, 214122, Jiangsu, China. jiasun@jiangnan.edu.cn.
Junjie XiaoCardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, 333 Nan Chen Road, Shanghai, 200444, China. junjiexiao@shu.edu.cn.
Shanghai University · CNJiangnan University · CNTongji Hospital · CNJiangsu Province Hospital · CNKarolinska Institutet · SEMassachusetts General Hospital · USNanjing Medical University · CNState Key Laboratory of Food Science and Technology · CNTongji University · CNUtrecht University · NL

Funding

Plasma miRNA predictors of adverse mechanical and electrical remodeling after MIUH3TR000901 · NCATS · MASSACHUSETTS GENERAL HOSPITAL · PI DAS, SAUMYA, KWONG, RAYMOND Y · 2015 to 2017
$3.2M
NCATS NIH HHS UH3 TR000901
6 · The paper itself

Abstract

backgroundCathelicidins are a major group of natural antimicrobial peptides which play essential roles in regulating host defense and immunity. In addition to the antimicrobial and immunomodulatory activities, recent studies have reported the involvement of cathelicidins in cardiovascular diseases by regulating inflammatory response and microvascular dysfunction. However, the role of cathelicidins in myocardial apoptosis upon cardiac ischemia/reperfusion (I/R) injury remains largely unknown.

methodsCRAMP (cathelicidin-related antimicrobial peptide) levels were measured in the heart and serum from I/R mice and in neonatal mouse cardiomyocytes treated with oxygen glucose deprivation/reperfusion (OGDR). Human serum cathelicidin antimicrobial peptide (LL-37) levels were measured in myocardial infarction (MI) patients. The role of CRAMP in myocardial apoptosis upon I/R injury was investigated in mice injected with the CRAMP peptide and in CRAMP knockout (KO) mice, as well as in OGDR-treated cardiomyocytes.

resultsWe observed reduced CRAMP level in both heart and serum samples from I/R mice and in OGDR-treated cardiomyocytes, as well as reduced LL-37 level in MI patients. Knockdown of CRAMP enhanced cardiomyocyte apoptosis, and CRAMP KO mice displayed increased infarct size and myocardial apoptosis. In contrast, the CRAMP peptide reduced cardiomyocyte apoptosis and I/R injury. The CRAMP peptide inhibited cardiomyocyte apoptosis by activation of Akt and ERK1/2 and phosphorylation and nuclear export of FoxO3a. c-Jun was identified as a negative regulator of the CRAMP gene. Moreover, lower level of serum LL-37/neutrophil ratio was associated with readmission and/or death in MI patients during 1-year follow-up.

conclusionsCRAMP protects against cardiomyocyte apoptosis and cardiac I/R injury via activation of Akt and ERK and phosphorylation and nuclear export of FoxO3a. Increasing LL-37 might be a novel therapy for cardiac ischemic injury.

Indexed as

AnimalsAnti-Infective AgentsCathelicidinsHumansMaleMiceMice, Inbred C57BLMice, KnockoutMyocardial Reperfusion InjuryAnti-Infective AgentsCathelicidinsApoptosisCardiomyocyteCathelicidinCRAMPIschemia/reperfusion injuryLL-37

Identifiers

PMID30782145
PMCPMC6381635
OpenAlexW2922429934

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.