Evidence map›Paper›PMID 33491670›Full record

ArticleJCI insight2021

Dysregulated SREBP1c/miR-153 signaling induced by hypertriglyceridemia worsens acute pancreatitis and delays tissue repair.

Juanjuan Dai, Mingjie Jiang, Yangyang Hu, Jingbo Xiao, Bin Hu, Jiyao Xu, Xiao Han, Shuangjun Shen, Bin Li, Zengkai Wu and 5 more

Abstract read
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Review
  3. Antioxidants (Basel, Switzerland) · 2025
    Article
  4. Article
  5. Identification of Novel 58-5p andInternational journal of molecular sciences · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. The Role of MicroRNAs in Pancreatitis Development and Progression.International journal of molecular sciences · 2023
    Review
  12. Review
  13. Review
  14. Review
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

15 authors.

Juanjuan DaiDepartment of Gastroenterology and.
Mingjie JiangShanghai Key Laboratory of Pancreatic Diseases, Shanghai General Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Yangyang HuDepartment of Gastroenterology and.
Jingbo XiaoDepartment of Gastroenterology and.
Bin HuDepartment of Gastroenterology and.
Jiyao XuDepartment of Emergency, Shanghai General Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Xiao HanDepartment of Gastroenterology and.
Shuangjun ShenDepartment of Gastroenterology and.
Bin LiDepartment of Gastroenterology and.
Zengkai WuDepartment of Gastroenterology and.
Yan HeDepartment of Gastroenterology and.
Yingchun RenDepartment of Gastroenterology and.
Li WenDepartment of Gastroenterology and.
Xingpeng WangDepartment of Gastroenterology and.
Guoyong HuDepartment of Gastroenterology and.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute pancreatitis (AP) is a life-threatening disease with up to 30% mortality. Therefore, prevention of AP aggravation and promotion of pancreatic regeneration are critical during the course and treatment of AP. Hypertriglyceridemia (HTG) is an established aggravating factor for AP that hinders pancreatic regeneration; however, its exact mechanism remains unclear. Using miRNA sequencing and further verification, we found that miRNA-153 (miR-153) was upregulated in the pancreas of HTG animal models and in the plasma of patients with HTG-AP. Increased miR-153 aggravated HTG-AP and delayed pancreatic repair via targeting TRAF3. Furthermore, miR-153 was transcriptionally suppressed by sterol regulatory element-binding transcription factor 1c (SREBP1c), which was suppressed by lipoprotein lipase malfunction-induced HTG. Overexpressing SREBP1c suppressed miR-153 expression, alleviated the severity of AP, and facilitated tissue regeneration in vivo. Finally, therapeutic administration of insulin also protected against HTG-AP via upregulating SREBP1c. Collectively, our results not only provide evidence that HTG leads to the development of more severe AP and hinders pancreatic regeneration via inducing persistent dysregulation of SREBP1c/miR-153 signaling, but also demonstrate that SREBP1c activators, including insulin, might be used to treat HTG-AP in patients.

Indexed as

AnimalsDisease Models, AnimalHumansHypertriglyceridemiaInsulinLipoprotein LipaseMaleMiceMice, Inbred C57BLMicroRNAsPancreasPancreatitisRatsRats, Sprague-DawleyRegenerationSignal TransductionInsulinLipoprotein LipaseMicroRNAsMIRN153 microRNA, humanMIRN153 microRNA, mouseMIRN153 microRNA, ratSREBF1 protein, humanSrebf1 protein, mouseSrebf1 protein, ratSterol Regulatory Element Binding Protein 1TNF Receptor-Associated Factor 3EpigeneticsGastroenterologyInsulinMolecular pathologyTherapeutics

Identifiers

PMID33491670
PMCPMC7934861

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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.