Evidence map›Paper›PMID 37039556›Full record

ArticleAutophagy2023

NR3C1/Glucocorticoid receptor activation promotes pancreatic β-cell autophagy overload in response to glucolipotoxicity.

Tijun Wu, Yixue Shao, Xirui Li, Tao Wu, Ling Yu, Jin Liang, Yaru Zhang, Jiahui Wang, Tong Sun, Yunxia Zhu and 4 more

Open access · greenAbstract read
In one paragraph

Article in Autophagy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
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  6. MedComm · 2026
    Article
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  11. Review
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  13. Progress on multifunctional transmembrane protein ATG9A.Cell communication and signaling : CCS · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Mechanistic Insights IntoDiabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Article
  19. Article
  20. 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

14 authors at 2 institutions in 1 country.

Tijun WuKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.ORCID 0000-0002-8788-5686
Yixue ShaoKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Xirui LiKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Tao WuKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Ling YuKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Jin LiangKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Yaru ZhangKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Jiahui WangKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Tong SunKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Yunxia ZhuKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Xiaoai ChangKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Shusen WangOrgan Transplant Center, Tianjin First Central Hospital, Nankai University, Tianjin, China.
Fang ChenKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Xiao HanKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.ORCID 0000-0002-6467-1802
Nanjing Medical University · CNNankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes is a complex and heterogeneous disorder characterized by chronic hyperglycemia. Its core cause is progressively impaired insulin secretion by pancreatic β-cell failures, usually upon a background of preexisting insulin resistance. Recent studies demonstrate that macroautophagy/autophagy is essential to maintain architecture and function of β-cells, whereas excessive autophagy is also involved in β-cell dysfunction and death. It has been poorly understood whether autophagy plays a protective or harmful role in β-cells, while we report here that it is dependent on NR3C1/glucocorticoid receptor activation. We proved that deleterious hyperactive autophagy happened only upon NR3C1 activation in β-cells under glucolipotoxic conditions, which eventually promoted diabetes. The transcriptome and the

Indexed as

Diabetes Mellitus, Type 2Insulin-Secreting CellsAlpha-Ketoglutarate-Dependent Dioxygenase FTOAnimalsAutophagyGlucocorticoidsGlucoseHumansMiceObesityReceptors, GlucocorticoidRNAAlpha-Ketoglutarate-Dependent Dioxygenase FTOFTO protein, humanGlucocorticoidsGlucoseNR3C1 protein, humanNR3C1 protein, mouseReceptors, GlucocorticoidRNAAutophagydiabetesFTOm6ANR3C1pancreatic β-cell

Identifiers

PMID37039556
PMCPMC10392762
OpenAlexW4364353241

What OpenQuestion holds

Textmetadata
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.