Evidence map›Paper›PMID 36305917›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2022

RCAN1 deficiency aggravates sepsis-induced cardiac remodeling and dysfunction by accelerating mitochondrial pathological fission.

Jinqiang Zhuang, Liming Chen, Gongke Li, Le Xia, Shaohong Wu, Junling Leng, Xuefei Tao, Jiang Hong, Yong Wu, Shijun Wang and 1 more

Abstract read
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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

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  11. [Enhanced endoplasmic reticulum RyR1 receptor phosphorylation leads to diaphragmatic dysfunction in septic rats].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
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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

11 authors at 6 institutions in 1 country.

Jinqiang Zhuang *Emergency Intensive Care Unit (EICU), The Affiliated Hospital of Yangzhou University, Yangzhou University, Jiangsu Province, 225000, China.
Liming Chen *Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Gongke LiEmergency Intensive Care Unit (EICU), The Affiliated Hospital of Yangzhou University, Yangzhou University, Jiangsu Province, 225000, China.
Le XiaEmergency Intensive Care Unit (EICU), The Affiliated Hospital of Yangzhou University, Yangzhou University, Jiangsu Province, 225000, China.
Shaohong WuDepartment of Critical Care Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201600, China.
Junling LengEmergency Intensive Care Unit (EICU), The Affiliated Hospital of Yangzhou University, Yangzhou University, Jiangsu Province, 225000, China.
Xuefei TaoSichuan Academy of Medical Science & Sichuan Provincial People's Hospital, Chengdu, China.
Jiang HongDepartment of Critical Care Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201600, China.
Yong WuDepartment of Cardiology, The Affiliated Hospital of Yangzhou University, Yangzhou University, Jiangsu Province, 225000, China. 13852786827@163.com.
Shijun WangShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. shijun_w@126.com.
Ruijun YuanDepartment of Cardiovascular Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China. dr_yuanrj@163.com.
Yangzhou University · CNShanghai Jiao Tong University · CNChanghai Hospital · CNFudan University · CNSichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CNSun Yat-sen University · CN

Funding

National Nature Science Foundation of China 82170255 and 81770274Shanghai Pujiang Program 21PJD013
6 · The paper itself

Abstract

objectiveCardiac dysfunction and remodeling are serious complications of sepsis and are the main causes of death in sepsis. RCAN1 is a feedback regulator of cardiac hypertrophy. Here, we aim to investigate the role of RCAN1 in septic cardiomyopathy.

methodsMice were randomly divided into control-WT, control-RCAN1

resultsOur data show that RCAN1 was downregulated in septic mouse heart and LPS-induced cardiomyocytes. RCAN1

conclusionsOur finding demonstrated that RCAN1 deficiency aggravated mitochondrial injury and septic cardiomyopathy through activating CaMKII. RCAN1 serves as a novel therapeutic target for treatment of sepsis-related cardiac remodeling and dysfunction.

Indexed as

CardiomyopathiesSepsisAnimalsBenzenesulfonamidesBenzylaminesCalcium-Calmodulin-Dependent Protein Kinase Type 2CardiomegalyDynaminsFibrosisLipopolysaccharidesMiceMyocytes, CardiacVentricular RemodelingBenzenesulfonamidesBenzylaminesCalcium-Calmodulin-Dependent Protein Kinase Type 2DynaminsKN 93LipopolysaccharidesCaMKIICardiac remodelingMitochondriaRCAN1Sepsis

Identifiers

PMID36305917
OpenAlexW4307498938

What OpenQuestion holds

Textmetadata
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.