Evidence map›Paper›PMID 35079095›Full record

ArticleCommunications biology2022

Intrinsic cardiac adrenergic cells contribute to LPS-induced myocardial dysfunction.

Duomeng Yang, Xiaomeng Dai, Yun Xing, Xiangxu Tang, Guang Yang, Andrew G Harrison, Jason Cahoon, Hongmei Li, Xiuxiu Lv, Xiaohui Yu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.3field-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

11 citing papers in PubMed, 24 citations in OpenAlex.

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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

12 authors at 2 institutions in 2 countries.

Duomeng Yang *Department of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.ORCID http://orcid.org/0000-0003-2937-7402
Xiaomeng Dai *Department of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Yun Xing *Department of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Xiangxu TangDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Guang YangDepartment of Pathogen biology, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Andrew G HarrisonDepartment of Immunology, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT, 06030, USA.
Jason CahoonDepartment of Immunology, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT, 06030, USA.
Hongmei LiDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Xiuxiu LvDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Xiaohui YuDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Penghua WangDepartment of Immunology, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT, 06030, USA.ORCID http://orcid.org/0000-0002-7332-1871
Huadong WangDepartment of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China. owanghd@jnu.edu.cn.ORCID http://orcid.org/0000-0002-2197-3624
Jinan University · CNUConn Health · US

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81871542
6 · The paper itself

Abstract

Intrinsic cardiac adrenergic (ICA) cells regulate both developing and adult cardiac physiological and pathological processes. However, the role of ICA cells in septic cardiomyopathy is unknown. Here we show that norepinephrine (NE) secretion from ICA cells is increased through activation of Toll-like receptor 4 (TLR4) to aggravate myocardial TNF-α production and dysfunction by lipopolysaccharide (LPS). In ICA cells, LPS activated TLR4-MyD88/TRIF-AP-1 signaling that promoted NE biosynthesis through expression of tyrosine hydroxylase, but did not trigger TNF-α production due to impairment of p65 translocation. In a co-culture consisting of LPS-treated ICA cells and cardiomyocytes, the upregulation and secretion of NE from ICA cells activated cardiomyocyte β

Indexed as

AnimalsCardiomyopathiesCardiovascular AgentsGene DeletionGene Expression RegulationLipopolysaccharidesMaleMiceMyocytes, CardiacNorepinephrineRatsRats, Sprague-DawleyToll-Like Receptor 4Cardiovascular AgentsLipopolysaccharidesNorepinephrineTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID35079095
PMCPMC8789803
OpenAlexW4206925387

What OpenQuestion 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 OpenQuestion graph.