Evidence map›Paper›PMID 33043596›Full record

ArticleJournal of cellular and molecular medicine2020

Calhex231 ameliorates myocardial fibrosis post myocardial infarction in rats through the autophagy-NLRP3 inflammasome pathway in macrophages.

Wenxiu Liu, Jiaxing Sun, Yutong Guo, Na Liu, Xue Ding, Xin Zhang, Jinyu Chi, Ningning Kang, Yue Liu, Xinhua Yin

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Cardioprotective Role of CalhexCell biochemistry and biophysics · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Review
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  8. Review
  9. The Role of Pyroptosis in Coronary Heart Disease.Anatolian journal of cardiology · 2024
    Article
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  11. Review
  12. 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

10 authors at 1 institution in 1 country.

Wenxiu LiuDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin, China.ORCID 0000-0002-8835-5556
Jiaxing SunDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Yutong GuoDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Na LiuDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Xue DingDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Xin ZhangDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Jinyu ChiDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Ningning KangDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Yue LiuDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin, China.ORCID 0000-0002-3192-6020
Xinhua YinDepartment of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin, China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The calcium-sensing receptor (CaSR) is involved in the pathophysiology of many cardiovascular diseases, including myocardial infarction (MI) and hypertension. The role of Calhex231, a specific inhibitor of CaSR, in myocardial fibrosis following MI is still unclear. Using Wistar rats, we investigated whether Calhex231 ameliorates myocardial fibrosis through the autophagy-NLRP3 inflammasome pathway in macrophages post myocardial infarction (MI). The rats were randomly divided into sham, MI and MI + Calhex231 groups. Compared with the sham rats, the MI rats consistently developed severe cardiac function, myocardial fibrosis and infiltration of inflammatory cells including macrophages. Moreover, inflammatory pathway including activation of NLRP3 inflammasome, IL-1β and autophagy was significantly up-regulated in myocardial tissue, infiltrated cardiac macrophages and peritoneal macrophages of the MI rats. These impacts were reversed by Calhex231. In vitro, studies revealed that calindol and rapamycin exacerbated MI-induced autophagy and NLRP3 inflammasome activation in peritoneal macrophages. Calhex231 and 3-Methyladenine (a specific inhibitor of autophagy) attenuated both autophagy and NLRP3 inflammasome activation; however, the caspase-1 inhibitor Z-YVAD-FMK did not. Our study indicated that Calhex231 improved cardiac function and ameliorated myocardial fibrosis post MI, likely via the inhibition of autophagy-mediated NLRP3 inflammasome activation; this provides a new therapeutic target for ventricular remodelling-related cardiovascular diseases.

Indexed as

AnimalsAutophagyBenzamidesBiomarkersCardiomyopathiesCyclohexylaminesDisease Models, AnimalFibrosisFluorescent Antibody TechniqueImmunohistochemistryInflammasomesMacrophagesMacrophages, PeritonealMaleMyocardial InfarctionNLR Family, Pyrin Domain-Containing 3 ProteinBenzamidesBiomarkersCyclohexylaminesInflammasomesN(1)-(4-chlorobenzoyl)-N(2)-(1-(1-naphthyl)ethyl)-1,2-diaminocyclohexaneNLR Family, Pyrin Domain-Containing 3 Proteinautophagycalcium-sensing receptormacrophagemyocardial infarctionNLRP3 inflammasome

Identifiers

PMID33043596
PMCPMC7701583
OpenAlexW3091893992

What OpenQuestion holds

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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 OpenQuestion graph.