Evidence map›Paper›PMID 32317756›Full record

ArticleActa pharmacologica Sinica2021

Cardamonin protects against lipopolysaccharide-induced myocardial contractile dysfunction in mice through Nrf2-regulated mechanism.

Ying Tan, Hong-Hong Wan, Ming-Ming Sun, Wen-Jing Zhang, Maolong Dong, Wei Ge, Jun Ren, Hu Peng

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
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  10. Nrf2 mediated signaling axis in sepsis-induced cardiomyopathy: potential Pharmacological receptor.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  14. DL-3-Heliyon · 2024
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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

8 authors at 4 institutions in 2 countries.

Ying Tan *Department of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Hong-Hong Wan *Department of Emergency, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Ming-Ming Sun *Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY, 82071, USA.
Wen-Jing ZhangDepartment of Emergency, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Maolong DongDepartment of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. 2206723777@qq.com.
Wei GeCenter for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY, 82071, USA. geweidr@fmmu.edu.cn.
Jun RenCenter for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY, 82071, USA. jren@uwyo.edu.
Hu PengDepartment of Emergency, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China. 1973denkepeng@tongji.edu.cn.
University of Wyoming · USTongji University · CNShanghai Tenth People's Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In patients with sepsis, lipopolysaccharide (LPS) from the outer membrane of gram-negative bacteria triggers cardiac dysfunction and heart failure, but target therapy for septic cardiomyopathy remains unavailable. In this study we evaluated the beneficial effects of cardamonin (CAR), a flavone existing in Alpinia plant, on endotoxemia-induced cardiac dysfunction and the underlying mechanisms with focus on oxidative stress and apoptosis. Adult mice were exposed to LPS (4 mg/kg, i.p. for 6 h) prior to functional or biochemical assessments. CAR (20 mg/kg, p.o.) was administered to mice immediately prior to LPS challenge. We found that LPS challenge compromised cardiac contractile function, evidenced by compromised fractional shortening, peak shortening, maximal velocity of shortening/relengthening, enlarged LV end systolic diameter and prolonged relengthening in echocardiography, and induced apoptosis, overt oxidative stress (O

Indexed as

AnimalsApoptosisCardiomyopathiesCardiotonic AgentsChalconesFemaleHeartInflammationLipopolysaccharidesMaleMiceMyocardial ContractionMyocardiumMyocytes, CardiacNF-E2-Related Factor 2NF-kappa B p50 SubunitcardamoninCardiotonic AgentsChalconesLipopolysaccharidesNfe2l2 protein, mouseNF-E2-Related Factor 2NF-kappa B p50 SubunitNfkb1 protein, mouseapoptosiscardamonincardiac dysfunctioninflammationlipopolysaccharideoxidative stress

Identifiers

PMID32317756
PMCPMC8027872
OpenAlexW3016647012

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.