Evidence map›Paper›PMID 29335338›Full record

ArticleEMBO molecular medicine2018

CRTH2 promotes endoplasmic reticulum stress-induced cardiomyocyte apoptosis through m-calpain.

Shengkai Zuo, Deping Kong, Chenyao Wang, Jiao Liu, Yuanyang Wang, Qiangyou Wan, Shuai Yan, Jian Zhang, Juan Tang, Qianqian Zhang and 6 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

45 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  7. Article
  8. Review
  9. Article
  10. TIGAR Suppresses ER Stress-Induced Neuronal Injury through Targeting ATF4 Signaling in Cerebral Ischemia/Reperfusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. The Link between Prostanoids and Cardiovascular Diseases.International journal of molecular sciences · 2023
    Review
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

16 authors at 5 institutions in 2 countries.

Shengkai ZuoDepartment of Pharmacology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Deping KongDepartment of Pharmacology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Chenyao WangKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.ORCID 0000-0002-0957-1956
Jiao LiuKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Yuanyang WangDepartment of Pharmacology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Qiangyou WanKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Shuai YanKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Jian ZhangDepartment of Pharmacology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Juan TangKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Qianqian ZhangKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Luheng LyuKey Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Xin LiDepartment of Pharmacology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Zhixin ShanMedical Research Department of Guangdong General Hospital, Guangdong Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou Guangdong, China.
Li QianMcAllister Heart Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Yujun ShenDepartment of Pharmacology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China yujun_shen@yahoo.com yuying@tmu.edu.cn.ORCID 0000-0002-9266-9064
Ying YuDepartment of Pharmacology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China yujun_shen@yahoo.com yuying@tmu.edu.cn.ORCID 0000-0002-6476-1752
Chinese Academy of Sciences · CNTianjin Medical University · CNGuangdong General Hospital · CNUniversity of Miami · USUniversity of North Carolina at Chapel Hill · US

Funding

Molecular mechanisms of direct cardiac reprogrammingR01HL128331 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI QIAN, LI · 2016 to 2020
$2.1M
NHLBI NIH HHS R01 HL128331
6 · The paper itself

Abstract

Apoptotic death of cardiac myocytes is associated with ischemic heart disease and chemotherapy-induced cardiomyopathy. Chemoattractant receptor-homologous molecule expressed on T helper type 2 cells (CRTH2) is highly expressed in the heart. However, its specific role in ischemic cardiomyopathy is not fully understood. Here, we demonstrated that CRTH2 disruption markedly improved cardiac recovery in mice postmyocardial infarction and doxorubicin challenge by suppressing cardiomyocyte apoptosis. Mechanistically, CRTH2 activation specifically facilitated endoplasmic reticulum (ER) stress-induced cardiomyocyte apoptosis via caspase-12-dependent pathway. Blockage of m-calpain prevented CRTH2-mediated cardiomyocyte apoptosis under ER stress by suppressing caspase-12 activity. CRTH2 was coupled with G

Indexed as

ApoptosisEndoplasmic Reticulum StressAnimalsBone MarrowCalciumCalpainCardiotonic AgentsCaspase 12Cell HypoxiaCellular ReprogrammingDoxorubicinEnzyme ActivationFibroblastsGene DeletionGTP-Binding Protein alpha Subunits, Gq-G11HumansCalciumCalpainCardiotonic AgentsCaspase 12DoxorubicinGTP-Binding Protein alpha Subunits, Gq-G11m-calpainProstaglandin D2prostaglandin D2 receptorReceptors, ImmunologicReceptors, ProstaglandinTetrazolescalpaincardiomyocyte apoptosisCRTH2endoplasmic reticulum stressprostaglandin D2

Identifiers

PMID29335338
PMCPMC5840549
OpenAlexW2783266677

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.