Evidence map›Paper›PMID 37923718›Full record

ArticleNature communications2023

Spliceosome component Usp39 contributes to hepatic lipid homeostasis through the regulation of autophagy.

Donghai Cui, Zixiang Wang, Qianli Dang, Jing Wang, Junchao Qin, Jianping Song, Xiangyu Zhai, Yachao Zhou, Ling Zhao, Gang Lu and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. RNA splicing in health and disease.Molecular biomedicine · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Autophagy in the liver.Autophagy reports · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
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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

16 authors at 6 institutions in 3 countries.

Donghai Cui *Key Laboratory of Experimental Teratology, Ministry of Education, School of Basic Medical Science, Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan, China.ORCID 0000-0002-6273-8129
Zixiang Wang *Key Laboratory of Experimental Teratology, Ministry of Education, School of Basic Medical Science, Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan, China.ORCID 0000-0001-5252-9764
Qianli DangKey Laboratory of Experimental Teratology, Ministry of Education, School of Basic Medical Science, Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan, China.ORCID 0000-0001-5495-3999
Jing WangKey Laboratory of Experimental Teratology, Ministry of Education, School of Basic Medical Science, Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan, China.ORCID 0000-0002-5098-6619
Junchao QinKey Laboratory of Experimental Teratology, Ministry of Education, School of Basic Medical Science, Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan, China.
Jianping SongDepartment of General Surgery, The Second Hospital, Shandong University, Jinan, China.ORCID 0000-0002-8047-8930
Xiangyu ZhaiDepartment of General Surgery, The Second Hospital, Shandong University, Jinan, China.
Yachao ZhouKey Laboratory of Experimental Teratology, Ministry of Education, School of Basic Medical Science, Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan, China.ORCID 0009-0007-8364-925X
Ling ZhaoKey Laboratory of Experimental Teratology, Ministry of Education, School of Basic Medical Science, Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan, China.
Gang LuCUHK-SDU Joint Laboratory on Reproductive Genetics, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Hongbin LiuCenter for Reproductive Medicine, Shandong University, Jinan, China.
Gang LiuNephrology Research Institute of Shandong University, The Second Hospital of Shandong University, Jinan, China.
Runping LiuSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Changshun ShaoInstitutes for Translational Medicine, State Key Laboratory of Radiation Medicine and Protection, Soochow University, Suzhou, China. shaoc@suda.edu.cn.ORCID 0000-0003-2618-9342
Xiyu ZhangKey Laboratory of Experimental Teratology, Ministry of Education, School of Basic Medical Science, Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan, China. xiyuzhang@sdu.edu.cn.ORCID 0000-0002-4313-9016
Zhaojian LiuKey Laboratory of Experimental Teratology, Ministry of Education, School of Basic Medical Science, Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan, China. liujian9782@sdu.edu.cn.ORCID 0000-0002-2542-0859
Shandong University · CNSecond Hospital of Shandong University · CNQilu Hospital of Shandong University · CNBeijing University of Chinese Medicine · CNChinese University of Hong Kong · HKSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulation of alternative splicing (AS) enables a single transcript to yield multiple isoforms that increase transcriptome and proteome diversity. Here, we report that spliceosome component Usp39 plays a role in the regulation of hepatocyte lipid homeostasis. We demonstrate that Usp39 expression is downregulated in hepatic tissues of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) subjects. Hepatocyte-specific Usp39 deletion in mice leads to increased lipid accumulation, spontaneous steatosis and impaired autophagy. Combined analysis of RNA immunoprecipitation (RIP-seq) and bulk RNA sequencing (RNA-seq) data reveals that Usp39 regulates AS of several autophagy-related genes. In particular, deletion of Usp39 results in alternative 5' splice site selection of exon 6 in Heat shock transcription factor 1 (Hsf1) and consequently its reduced expression. Importantly, overexpression of Hsf1 could attenuate lipid accumulation caused by Usp39 deficiency. Taken together, our findings indicate that Usp39-mediated AS is required for sustaining autophagy and lipid homeostasis in the liver.

Indexed as

Non-alcoholic Fatty Liver DiseaseSpliceosomesAnimalsAutophagyHomeostasisHumansLipidsLiverMiceMice, Inbred C57BLUbiquitin-Specific ProteasesLipidsUbiquitin-Specific ProteasesUsp39 protein, mouse

Identifiers

PMID37923718
PMCPMC10624899
OpenAlexW4388300307

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.