Evidence map›Paper›PMID 39495216›Full record

ArticleeLife2024

Nuclear translocation of SIRT4 mediates deacetylation of U2AF2 to modulate renal fibrosis through alternative splicing-mediated upregulation of CCN2.

Guangyan Yang, Jiaqing Xiang, Xiaoxiao Yang, Xiaomai Liu, Yanchun Li, Lixing Li, Lin Kang, Zhen Liang, Shu Yang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Sirt4 Deficiency Promotes Cardiomyocyte Proliferation and Cardiac Repair.Journal of cellular and molecular medicine · 2025
    Article
  4. Review
  5. Article
  6. Lock out SIRT4.eLife · 2024
    Article
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

9 authors.

Guangyan Yang *Department of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Guangdong, China.
Jiaqing Xiang *Department of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Guangdong, China.
Xiaoxiao Yang *Anhui Provincial International Science and Technology Cooperation Base for Major Metabolic Diseases and Nutritional Interventions, Key Laboratory of Metabolism and Regulation for Major Diseases of Anhui Higher Education Institutes, College of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Xiaomai LiuDepartment of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Guangdong, China.
Yanchun LiDepartment of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Guangdong, China.
Lixing LiDepartment of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Guangdong, China.
Lin KangDepartment of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Guangdong, China.
Zhen LiangDepartment of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Guangdong, China.
Shu YangDepartment of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Guangdong, China.ORCID https://orcid.org/0000-0002-4912-777X

Funding

Key Program Topics of Shenzhen Basic Research JCYJ20220818102605013National Natural Science Foundation of China 82170842National Natural Science Foundation of China 82171556National Natural Science Foundation of China 82370876National Natural Science Foundation of China 82371572
6 · The paper itself

Abstract

TGF-β stimulates CCN2 expression which in turn amplifies TGF-β signaling. This process promotes extracellular matrix production and accelerates the pathological progression of fibrotic diseases. Alternative splicing plays an important role in multiple disease development, while U2 small nuclear RNA auxiliary factor 2 (U2AF2) is an essential factor in the early steps of pre-mRNA splicing. However, the molecular mechanism underlying abnormal

Indexed as

Alternative SplicingConnective Tissue Growth FactorFibrosisMitochondrial ProteinsSirtuinsSplicing Factor U2AFUp-RegulationAcetylationAnimalsCell NucleusHumansKidneyKidney DiseasesMaleMiceMice, Inbred C57BLCCN2 protein, humanCCN2 protein, mouseConnective Tissue Growth FactorMitochondrial ProteinsSIRT4 protein, mouseSirtuinsSplicing Factor U2AFTransforming Growth Factor betaCCN2cell biologykidney fibrosismousepre-mRNA splicingSIRT4U2AF2U2 snRNP

Identifiers

PMID39495216
PMCPMC11534337

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.