Evidence map›Paper›PMID 33101708›Full record

ArticleCell death discovery2020

Cardiomyocyte-restricted high-mobility group box 1 (HMGB1) deletion leads to small heart and glycolipid metabolic disorder through GR/PGC-1α signalling.

Peng Yu, Ming Liu, Baoli Zhang, Ying Yu, Enyong Su, Shiyao Xie, Lei Zhang, Xue Yang, Hong Jiang, Ruizhen Chen and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 9 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 1 country.

Peng Yu *Department of Endocrinology and Metabolism, Fudan Institute of Metabolic Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID 0000-0003-4942-7139
Ming Liu *Department of General Practice, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, China.
Baoli ZhangShanghai Institute of Cardiovascular Diseases, Shanghai Clinical Bioinformatics Research Institute, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, China.
Ying YuDepartment of General Practice, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, China.
Enyong SuShanghai Institute of Cardiovascular Diseases, Shanghai Clinical Bioinformatics Research Institute, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, China.
Shiyao XieShanghai Institute of Cardiovascular Diseases, Shanghai Clinical Bioinformatics Research Institute, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, China.
Lei ZhangShanghai Institute of Cardiovascular Diseases, Shanghai Clinical Bioinformatics Research Institute, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, China.
Xue YangShanghai Institute of Cardiovascular Diseases, Shanghai Clinical Bioinformatics Research Institute, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, China.
Hong JiangShanghai Institute of Cardiovascular Diseases, Shanghai Clinical Bioinformatics Research Institute, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0002-7260-9646
Ruizhen ChenShanghai Institute of Cardiovascular Diseases, Shanghai Clinical Bioinformatics Research Institute, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, China.
Yunzeng ZouShanghai Institute of Cardiovascular Diseases, Shanghai Clinical Bioinformatics Research Institute, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, China.
Junbo GeShanghai Institute of Cardiovascular Diseases, Shanghai Clinical Bioinformatics Research Institute, Zhongshan Hospital, Shanghai Medical College of Fudan University, Shanghai, China.
Shanghai Medical College of Fudan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac growth and remodelling are key biological processes influencing the physiological performance of the heart, and a previous study showed a critical role for intracellular HMGB1 in vitro. However, the in vivo study, which used conditional Hmgb1 ablation, did not show a significant effect on cellular or organic function. We have demonstrated the extracellular effect of HMGB1 as a pro-inflammatory molecule on cardiac remodelling. In this study, we found that HMGB1 deletion by cTnT-Cre in mouse hearts altered glucocorticoid receptor (GR) function and glycolipid metabolism, eventually leading to growth retardation, small heart and heart failure. The subcellular morphology did not show a significant change caused by HMGB1 knockout. The heart showed significant elevation of glycolysis, free fatty acid deposition and related enzyme changes. Transcriptomic analysis revealed a list of differentially expressed genes that coincide with glucocorticoid receptor function in neonatal mice and a significant increase in inflammatory genes in adult mice. Cardiac HMGB1 knockout led to a series of changes in PGC-1α, UCP3 and GyK, which were the cause of metabolic changes and further impacted cardiac function. Ckmm-Cre Hmgb1

Indexed as

Developmental biologyHeart failure

Identifiers

PMID33101708
PMCPMC7575537
OpenAlexW3093561520

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.