Evidence map›Paper›PMID 34697288›Full record

ArticleCell death & disease2021

Lnc-PFAR facilitates autophagy and exacerbates pancreatic fibrosis by reducing pre-miR-141 maturation in chronic pancreatitis.

Tao Zhang, Guangquan Zhang, Wenbo Yang, Hongze Chen, Jisheng Hu, Zhongjie Zhao, Chundong Cheng, Guanqun Li, Yu Xie, Yilong Li and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
8.2field-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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  5. PdgfrαGenes & diseases · 2025
    Review
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  7. Article
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  9. Article
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  12. Article
  13. Article
  14. Article
  15. The Role of MicroRNAs in Pancreatitis Development and Progression.International journal of molecular sciences · 2023
    Review
  16. Review
  17. Article
  18. Review
  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

18 authors at 1 institution in 1 country.

Tao Zhang *Department of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0003-1244-2116
Guangquan Zhang *Department of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0002-4803-0693
Wenbo YangDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0002-4380-2236
Hongze ChenDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0002-4805-4150
Jisheng HuDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0003-4550-4897
Zhongjie ZhaoDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0003-0213-0426
Chundong ChengDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0001-7014-3611
Guanqun LiDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Yu XieDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0001-5518-3973
Yilong LiDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0002-3911-2830
Rui KongDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0002-6863-3125
Yongwei WangDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Gang WangDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0002-1186-4336
Hua ChenDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0002-6726-791X
Xue-Wei BaiDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.ORCID 0000-0001-8015-5464
Shangha PanKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Harbin, Heilongjiang, China.ORCID 0000-0003-0554-8684
Bei SunDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. sunbei70@tom.com.ORCID 0000-0001-6688-2294
Le LiDepartment of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. lile@hrbmu.edu.cn.ORCID 0000-0002-5610-2343
Harbin Medical University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81670583National Natural Science Foundation of China (National Science Foundation of China) 81702384National Natural Science Foundation of China (National Science Foundation of China) 81800572National Natural Science Foundation of China (National Science Foundation of China) 81871974
6 · The paper itself

Abstract

Chronic pancreatitis (CP) is described as progressive inflammatory fibrosis of pancreas, accompanied with irreversible impaired endocrine and exocrine insufficiency. Pancreatic stellate cells (PSCs) are widely distributed in the stroma of the pancreas and PSCs activation has been shown as one of the leading causes for pancreatic fibrosis. Our previous study has revealed that autophagy is dramatically activated in CP tissues, which facilitates PSCs activation and pancreatic fibrosis. Long non-coding RNAs (LncRNAs) have been recognized as crucial regulators for fibrosis-related diseases. LncRNAs interact with RNA binding protein or construct competitive endogenous RNA (ceRNA) hypothesis which elicited the fibrotic processes. Until now, the effects of lncRNAs on PSCs activation and pancreatic fibrosis have not been clearly explored. In this study, a novel lncRNA named Lnc-PFAR was found highly expressed in mouse and human CP tissues. Our data revealed that Lnc-PFAR facilitates PSCs activation and pancreatic fibrosis via RB1CC1-induced autophagy. Lnc-PFAR reduces miR-141 expression by suppressing pre-miR-141 maturation, which eventually upregulates the RB1CC1 and fibrosis-related indicators expression. Meanwhile, Lnc-PFAR enhanced PSCs activation and pancreatic fibrosis through trigging autophagy. Our study interrogates a novel lncRNA-induced mechanism in promoting the development of pancreatic fibrosis, and Lnc-PFAR is suggested to be a prospective therapeutic target in clinical scenarios.

Indexed as

AnimalsAutophagyCase-Control StudiesChronic DiseaseDisease Models, AnimalFibrosisHumansMiceMicroRNAsPancreatitis, ChronicRNA, Long NoncodingMicroRNAsMirn141 microRNA, mouseRNA, Long Noncoding

Identifiers

PMID34697288
PMCPMC8547218
OpenAlexW3211252854

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.