Evidence map›Paper›PMID 36179018›Full record

ArticleScience advances2022

Regulation of autoimmune disease progression by Pik3ip1 through metabolic reprogramming in T cells and therapeutic implications.

Wenqiang Xie, Juan Fang, Zhongyan Shan, Junyi Guo, Yuan Liao, Zhaolei Zou, Jun Wang, Shuqiong Wen, Lisa Yang, Yanshu Zhang and 6 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  5. Article
  6. Review
  7. Article
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  10. Review
  11. Article
  12. Article
  13. Article
  14. Metabolic Reprogramming of CD4International journal of nanomedicine · 2024
    Article
  15. The Wheel of p53 Helps to Drive the Immune System.International journal of molecular sciences · 2023
    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

16 authors at 5 institutions in 2 countries.

Wenqiang XieGuanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Stomatological Hospital, Sun Yat-Sen University, Guangzhou 510055, China.ORCID 0000-0002-3888-8733
Juan FangGuanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Stomatological Hospital, Sun Yat-Sen University, Guangzhou 510055, China.ORCID 0000-0002-0207-3436
Zhongyan ShanGuanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Stomatological Hospital, Sun Yat-Sen University, Guangzhou 510055, China.ORCID 0000-0002-9141-0675
Junyi GuoGuanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Stomatological Hospital, Sun Yat-Sen University, Guangzhou 510055, China.
Yuan LiaoDepartment of Laboratory Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Zhaolei ZouGuanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Stomatological Hospital, Sun Yat-Sen University, Guangzhou 510055, China.ORCID 0000-0001-7577-3436
Jun WangDepartment of Pathology, New York University Grossman School of Medicine, New York, NY, USA.ORCID 0000-0002-6346-2929
Shuqiong WenGuanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Stomatological Hospital, Sun Yat-Sen University, Guangzhou 510055, China.
Lisa YangGuanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Stomatological Hospital, Sun Yat-Sen University, Guangzhou 510055, China.
Yanshu ZhangGuanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Stomatological Hospital, Sun Yat-Sen University, Guangzhou 510055, China.ORCID 0000-0002-0799-877X
Huanzi LuGuanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Stomatological Hospital, Sun Yat-Sen University, Guangzhou 510055, China.ORCID 0000-0001-5243-9611
Hang ZhaoState Key Laboratory of Oral Diseases, Chinese Academy of Medical Sciences Research Unit of Oral Carcinogenesis and Management, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Dong-Ming KuangKey Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.ORCID 0000-0003-3570-9717
Peng HuangSun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.ORCID 0000-0002-2152-9152
Qianming ChenSchool of Stomatology, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0002-5371-4432
Zhi WangGuanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Stomatological Hospital, Sun Yat-Sen University, Guangzhou 510055, China.ORCID 0000-0002-5276-1413
Guangdong Province Stomatological Hospital · CNSun Yat-sen University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNNew York University · USZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic alterations could profoundly affect immune functions and influence the progression and outcome of autoimmune diseases. However, the detailed mechanisms and their therapeutic potential remain to be defined. Here, we show that phosphatidylinositide 3-kinase interacting protein 1 (Pik3ip1), a newly identified negative immune regulator, is notably down-regulated in several major autoimmune diseases through a previously unidentified mechanism mediated by interleukin-21/p38 mitogen-activated protein kinase/a disintegrin and metalloprotease-17 (ADAM17) pathway. Down-regulation of Pik3ip1 in T cells causes a major metabolic shift from oxidative phosphorylation toward aerobic glycolysis, leading to their overactivation and aggressive disease progression in experimental autoimmune encephalomyelitis (EAE) mouse model. Suppression of hypoxia-inducible factor 1α (Hif1α) or pharmacologic inhibition of glycolysis could reverse these phenotypes and largely mitigate EAE severity. Our study reveals a previously unrecognized role of Pik3ip1 in metabolic regulation that substantially affects the inflammatory loop in the autoimmune setting and identifies the Pik3ip1/Hif1α/glycolysis axis as a potential therapeutic target for treatment of autoimmune diseases.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalT-LymphocytesAnimalsDisease ProgressionDisintegrinsIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicep38 Mitogen-Activated Protein KinasesDisintegrinsIntracellular Signaling Peptides and ProteinsMembrane Proteinsp38 Mitogen-Activated Protein KinasesPik3ip1 protein, mouse

Identifiers

PMID36179018
PMCPMC9524833
OpenAlexW4298126230

What OpenQuestion holds

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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.