Evidence map›Paper›PMID 35398277›Full record

ArticleMolecular metabolism2022

Autotaxin signaling facilitates β cell dedifferentiation and dysfunction induced by Sirtuin 3 deficiency.

Huanyi Cao, Arthur C K Chung, Xing Ming, Dandan Mao, Heung Man Lee, Xiaoyun Cao, Guy A Rutter, Juliana C N Chan, Xiao Yu Tian, Alice P S Kong

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Roles of SIRT3 in aging and aging-related diseases.International journal of biological sciences · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. 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

10 authors.

Huanyi CaoDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China; Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China.
Arthur C K ChungDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China.
Xing MingDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China; Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China.
Dandan MaoDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China; Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China.
Heung Man LeeDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China; Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China; Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong SAR, China.
Xiaoyun CaoSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China.
Guy A RutterCR-CHUM and Université de Montréal, Montréal, QC, Canada; Section of Cell Biology and Functional Genomics, Division of Diabetes, Endocrinology and Metabolism, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK; Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore.
Juliana C N ChanDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China; Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China; Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong SAR, China.
Xiao Yu TianSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China. Electronic address: xytian@cuhk.edu.hk.
Alice P S KongDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China; Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China; Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong SAR, China. Electronic address: alicekong@cuhk.edu.hk.

Funding

Medical Research Council MR/R022259/1Wellcome Trust 212625/Z/18/Z
6 · The paper itself

Abstract

objectiveβ cell dedifferentiation may underlie the reversible reduction in pancreatic β cell mass and function in type 2 diabetes (T2D). We previously reported that β cell-specific Sirt3 knockout (Sirt3

methodsWe applied LPA, or lysophosphatidylcoline (LPC), the substrate of ATX for producing LPA, to MIN6 cell line and mouse islets with altered Sirt3 expression to investigate the effect of LPA on β cell dedifferentiation and its underlying mechanisms. To examine the pathological effects of ATX/LPA pathway, we injected the β cell selective adeno-associated virus (AAV-Atx-shRNA) or negative control AAV-scramble in Sirt3

resultsIn Sirt3

conclusionsSirt3 prevents β cell dedifferentiation by inhibiting ATX expression and upregulation of LPA. These findings support a long-range signaling effect of Sirt3 which modulates the ATX-LPA pathway to reverse β cell dysfunction associated with glucolipotoxicity.

Indexed as

Diabetes Mellitus, Type 2Insulin-Secreting CellsAnimalsCell DedifferentiationGlucoseMicep38 Mitogen-Activated Protein KinasesSirtuin 3Glucosep38 Mitogen-Activated Protein KinasesSirt3 protein, mouseSirtuin 3AutotaxinLysophosphatidic acidMitogen-activated protein kinasesSirtuin3Type 2 diabetesβ cell dedifferentiation

Identifiers

PMID35398277
PMCPMC9048116

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.