Evidence map›Paper›PMID 35761309›Full record

ArticleDiabetology & metabolic syndrome2022

Targeting ferroptosis with miR-144-3p to attenuate pancreatic β cells dysfunction via regulating USP22/SIRT1 in type 2 diabetes.

Shanshan Zhang, Xiao Liu, Jihong Wang, Fengjuan Yuan, Yali Liu

Open access · goldAbstract read
In one paragraph

Article in Diabetology & metabolic syndrome, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  7. AAT-MSC-EVs: Novel implications for suppressing ferroptosis, fibrosis and pain associated with chronic pancreatitis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Potential role of SIRT1 in cell ferroptosis.Frontiers in cell and developmental biology · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. The role of regulated necrosis in diabetes and its complications.Journal of molecular medicine (Berlin, Germany) · 2024
    Review
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  19. 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

5 authors at 2 institutions in 2 countries.

Shanshan ZhangSchool of Medicine of Pingdingshan University, Middle Section of Chongwen Road, Xincheng District, Pingdingshan, 467000, Henan, China.
Xiao LiuSchool of Medicine of Pingdingshan University, Middle Section of Chongwen Road, Xincheng District, Pingdingshan, 467000, Henan, China. sszh.baobao@163.com.
Jihong WangSchool of Medicine of Pingdingshan University, Middle Section of Chongwen Road, Xincheng District, Pingdingshan, 467000, Henan, China. 799981507@qq.com.
Fengjuan YuanSchool of Medicine of Pingdingshan University, Middle Section of Chongwen Road, Xincheng District, Pingdingshan, 467000, Henan, China.
Yali LiuSchool of Medicine of Pingdingshan University, Middle Section of Chongwen Road, Xincheng District, Pingdingshan, 467000, Henan, China.
Pingdingshan University · CNPhilippine Women's University · PH

Funding

medical education research project of Henan Province, based on the construction of the elderly nursing technology curriculum system based on the post competency training of elderly nursing talents, project number wjlx2020293Pingdingshan University Health Assessment School-level Excellent Online Open Course jpzx19247
6 · The paper itself

Abstract

backgroundRecently, ferroptosis has been implicated in the pathologic process of several diseases including type 2 diabetes mellitus (T2DM). However, molecular mechanisms underlying ferroptosis in T2DM remain obscure.

methodsTwenty four mice were included in this study. T2DM model mice were established by a high-fat diet combined with streptozotocin injection. INS-1 cells were stimulated with high glucose (HG). Cell viability was detected by CCK-8 kit. The levels of GSH, MDA, iron, and lipid ROS, and SOD activity, were detected by the corresponding kits. The interaction between miR-144-3p and USP22 was validated by dual-luciferase reporter assay. The relationship between USP22 and its substrate was verified using Co-IP and ubiquitination assays. The mRNA and protein expressions were examined by RT-qPCR and western blot, respectively. The functions of β cells in vitro and in vivo were evaluated glucose-stimulated insulin secretion test and HOMA-β, respectively.

resultsFerroptosis occurred in the pancreas of T2DM mice and HG-induced INS-1 cells. Silencing miR-144-3p blocked the effect of HG on the cell viability and accumulation of lipid peroxides, thereby improving the insulin secretion in INS-1 cells. Mechanistically, USP22 is a direct target of miR-144-3p, which could stabilize SIRT1 expression, thereby suppressing ferroptosis. Overexpressing USP22 attenuated deleterious roles of HG in INS-1 cells; but its roles were reversed by up-regulating miR-144-3p. In vivo study demonstrated that miR-144-3p antagomir exerted an anti-hyperglycemic effect and regulated the ferroptosis-related proteins in the pancreas.

conclusionThe up-regulation of miR-144-3p suppressed USP22/SIRT1 to induce ferroptosis, which causes pancreatic β cells dysfunction, thereby promoting T2DM development.

Indexed as

FerroptosismiR-144-3pPancreatic β cellsType 2 diabetes mellitusUSP22

Identifiers

PMID35761309
PMCPMC9235078
OpenAlexW4283590418

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.