Evidence map›Paper›PMID 33436548›Full record

ArticleCell death & disease2021

Rosuvastatin protects against coronary microembolization-induced cardiac injury via inhibiting NLRP3 inflammasome activation.

Ao Chen, Zhangwei Chen, You Zhou, Yuan Wu, Yan Xia, Danbo Lu, Mengkang Fan, Su Li, Jinxiang Chen, Aijun Sun and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 50 citations in OpenAlex.

  1. Evolocumab for prevention of microvascular dysfunction in patients undergoing percutaneous coronary intervention: the randomised, open-label EVOCATION trial.EuroIntervention : journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology · 2022
    Trial
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  9. Vericiguat reduces pyroptosis in rats with coronary microembolization by inhibiting the AMPK/Nrf2/NLRP3 signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
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  20. Statins and Cardiomyocyte Metabolism, Friend or Foe?Journal of cardiovascular development and disease · 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

13 authors at 1 institution in 1 country.

Ao Chen *Department of Cardiology, Zhongshan Hospital, Fudan University; Shanghai Institute of Cardiovascular Diseases; National Clinical Research Center for Interventional Medicine, Shanghai, China.ORCID http://orcid.org/0000-0002-2577-522X
Zhangwei Chen *Department of Cardiology, Zhongshan Hospital, Fudan University; Shanghai Institute of Cardiovascular Diseases; National Clinical Research Center for Interventional Medicine, Shanghai, China.
You ZhouDepartment of Cardiology, Zhongshan Hospital, Fudan University; Shanghai Institute of Cardiovascular Diseases; National Clinical Research Center for Interventional Medicine, Shanghai, China.
Yuan WuDepartment of Cardiology, Zhongshan Hospital, Fudan University; Shanghai Institute of Cardiovascular Diseases; National Clinical Research Center for Interventional Medicine, Shanghai, China.
Yan XiaDepartment of Cardiology, Zhongshan Hospital, Fudan University; Shanghai Institute of Cardiovascular Diseases; National Clinical Research Center for Interventional Medicine, Shanghai, China.
Danbo LuDepartment of Cardiology, Zhongshan Hospital, Fudan University; Shanghai Institute of Cardiovascular Diseases; National Clinical Research Center for Interventional Medicine, Shanghai, China.
Mengkang FanDepartment of Cardiology, Zhongshan Hospital, Fudan University; Shanghai Institute of Cardiovascular Diseases; National Clinical Research Center for Interventional Medicine, Shanghai, China.
Su LiDepartment of Cardiology, Zhongshan Hospital, Fudan University; Shanghai Institute of Cardiovascular Diseases; National Clinical Research Center for Interventional Medicine, Shanghai, China.
Jinxiang ChenDepartment of Cardiology, Zhongshan Hospital, Fudan University; Shanghai Institute of Cardiovascular Diseases; National Clinical Research Center for Interventional Medicine, Shanghai, China.
Aijun SunDepartment of Cardiology, Zhongshan Hospital, Fudan University; Shanghai Institute of Cardiovascular Diseases; National Clinical Research Center for Interventional Medicine, Shanghai, China.
Yunzeng ZouDepartment of Cardiology, Zhongshan Hospital, Fudan University; Shanghai Institute of Cardiovascular Diseases; National Clinical Research Center for Interventional Medicine, Shanghai, China.
Juying QianDepartment of Cardiology, Zhongshan Hospital, Fudan University; Shanghai Institute of Cardiovascular Diseases; National Clinical Research Center for Interventional Medicine, Shanghai, China. qian.juying@zs-hospital.sh.cn.ORCID http://orcid.org/0000-0002-7512-3692
Junbo GeDepartment of Cardiology, Zhongshan Hospital, Fudan University; Shanghai Institute of Cardiovascular Diseases; National Clinical Research Center for Interventional Medicine, Shanghai, China. jbge@zs-hospital.sh.cn.ORCID http://orcid.org/0000-0001-9640-8171
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronary microembolization (CME), a common reason for periprocedural myocardial infarction (PMI), bears very important prognostic implications. However, the molecular mechanisms related to CME remain largely elusive. Statins have been shown to prevent PMI, but the underlying mechanism has not been identified. Here, we examine whether the NLRP3 inflammasome contributes to CME-induced cardiac injury and investigate the effects of statin therapy on CME. In vivo study, mice with CME were treated with 40 mg/kg/d rosuvastatin (RVS) orally or a selective NLRP3 inflammasome inhibitor MCC950 intraperitoneally (20 mg/kg/d). Mice treated with MCC950 and RVS showed improved cardiac contractile function and morphological changes, diminished fibrosis and microinfarct size, and reduced serum lactate dehydrogenase (LDH) level. Mechanistically, RVS decreased the expression of NLRP3, caspase-1, interleukin-1β, and Gasdermin D N-terminal domains. Proteomics analysis revealed that RVS restored the energy metabolism and oxidative phosphorylation in CME. Furthermore, reduced reactive oxygen species (ROS) level and alleviated mitochondrial damage were observed in RVS-treated mice. In vitro study, RVS inhibited the activation of NLRP3 inflammasome induced by tumor necrosis factor α plus hypoxia in H9c2 cells. Meanwhile, the pyroptosis was also suppressed by RVS, indicated by the increased cell viability, decreased LDH and propidium iodide uptake in H9c2 cells. RVS also reduced the level of mitochondrial ROS generation in vitro. Our results indicate the NLRP3 inflammasome-dependent cardiac pyroptosis plays an important role in CME-induced cardiac injury and its inhibitor exerts cardioprotective effect following CME. We also uncover the anti-pyroptosis role of RVS in CME, which is associated with regulating mitochondrial ROS.

Indexed as

AnimalsAnticholesteremic AgentsHumansInflammasomesMaleMiceMyocardial Reperfusion InjuryNLR Family, Pyrin Domain-Containing 3 ProteinRosuvastatin CalciumAnticholesteremic AgentsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinRosuvastatin Calcium

Identifiers

PMID33436548
PMCPMC7804109
OpenAlexW3118673276

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.