Evidence map›Paper›PMID 36653355›Full record

ArticleCell death discovery2023

HDAC1 disrupts the tricarboxylic acid (TCA) cycle through the deacetylation of Nur77 and promotes inflammation in ischemia-reperfusion mice.

Zhenhua Wu, Yunpeng Bai, Yujuan Qi, Chao Chang, Yan Jiao, Yaobang Bai, Zhigang Guo

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2023. 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
2.2field-weighted citation impact, top 13% 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, 15 citations in OpenAlex.

  1. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
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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

7 authors at 2 institutions in 1 country.

Zhenhua Wu *Academy of Medical Engineering and Translational Medicine, Tianjin University, 300222, Tianjin, China.
Yunpeng Bai *Department of Cardiac Surgery, Tianjin Chest Hospital, 300222, Tianjin, China.
Yujuan QiICU, Department of Cardiac Surgery, Tianjin Chest Hospital, 300222, Tianjin, China.
Chao ChangICU, Department of Cardiac Surgery, Tianjin Chest Hospital, 300222, Tianjin, China.
Yan JiaoICU, Department of Cardiac Surgery, Tianjin Chest Hospital, 300222, Tianjin, China.
Yaobang BaiICU, Department of Cardiac Surgery, Tianjin Chest Hospital, 300222, Tianjin, China.
Zhigang GuoAcademy of Medical Engineering and Translational Medicine, Tianjin University, 300222, Tianjin, China. 1220235018@tju.edu.cn.ORCID http://orcid.org/0000-0003-4206-9877
Tianjin Chest Hospital · CNTianjin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylase enzymes (HDACs) regulate protein acetylation. HDAC1 is known to enhance ischemia/reperfusion (I/R) injury, but its underlying mechanism(s) of action have not been defined. Here, in vivo mouse models of myocardial I/R were used to investigate the role of HDAC1 during I/R myocardial injury. We show that HDAC1 enhances the inflammatory responses of I/R mice. Using a constructed macrophage H/R (hypoxia/ regeneration) injury model (Raw264.7 cells), we identified Nur77 as a HDAC1 target in macrophages. Nur77 deficient macrophages failed to downregulate IDH1 (isocitrate dehydrogenase 1) and accumulated succinic acid and other tricarboxylic acid (TCA) cycle-derived metabolites in a glutamine-independent manner. These data show that the inhibition of HDAC1 ameliorates H/R-inflammation in macrophages through the regulation of Nur77 and the TCA cycle.

Identifiers

PMID36653355
PMCPMC9849262
OpenAlexW4317207811

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.