Evidence map›Paper›PMID 36329235›Full record

ArticleCell death and differentiation2023

Blockage of PPARγ T166 phosphorylation enhances the inducibility of beige adipocytes and improves metabolic dysfunctions.

Nanfei Yang, Yuxin Wang, Qiang Tian, Qiuping Wang, Yan Lu, Luchen Sun, Sijie Wang, Yuncheng Bei, Jianguo Ji, Hu Zhou and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2023. 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
1.7field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 15 citations in OpenAlex.

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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

17 authors at 6 institutions in 2 countries.

Nanfei YangState Key Laboratory of Pharmaceutical Biotechnology, Department of Rheumatology and Immunology, The Affiliated Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, School of Life Sciences, Nanjing University, Nanjing, 210023, China.
Yuxin WangState Key Laboratory of Pharmaceutical Biotechnology, Department of Rheumatology and Immunology, The Affiliated Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, School of Life Sciences, Nanjing University, Nanjing, 210023, China.ORCID 0000-0002-3245-6665
Qiang TianState Key Laboratory of Pharmaceutical Biotechnology, Department of Rheumatology and Immunology, The Affiliated Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, School of Life Sciences, Nanjing University, Nanjing, 210023, China.
Qiuping WangState Key Laboratory of Pharmaceutical Biotechnology, Department of Rheumatology and Immunology, The Affiliated Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, School of Life Sciences, Nanjing University, Nanjing, 210023, China.
Yan LuState Key Laboratory of Pharmaceutical Biotechnology, Department of Rheumatology and Immunology, The Affiliated Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, School of Life Sciences, Nanjing University, Nanjing, 210023, China.
Luchen SunState Key Laboratory of Pharmaceutical Biotechnology, Department of Rheumatology and Immunology, The Affiliated Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, School of Life Sciences, Nanjing University, Nanjing, 210023, China.
Sijie WangState Key Laboratory of Pharmaceutical Biotechnology, Department of Rheumatology and Immunology, The Affiliated Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, School of Life Sciences, Nanjing University, Nanjing, 210023, China.
Yuncheng BeiState Key Laboratory of Pharmaceutical Biotechnology, Department of Rheumatology and Immunology, The Affiliated Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, School of Life Sciences, Nanjing University, Nanjing, 210023, China.
Jianguo JiState Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University, Beijing, 100871, China.
Hu ZhouDepartment of Analytical Chemistry and CAS Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zuchongzhi Road, Shanghai, 201203, China.ORCID 0000-0001-7006-4737
Wei YangDepartment of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, 90095, USA.ORCID 0000-0003-2575-3570
Pengju YaoState Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University, Beijing, 100871, China.
Wenyuan ZhuState Key Laboratory of Protein and Plant Gene Research, School of Life Sciences, Peking University, Beijing, 100871, China.
Lingyun SunDepartment of Rheumatology and Immunology, the Affiliated Drum Tower Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, China.
Zhifeng HuangOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health) & School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.ORCID 0000-0001-8269-6731
Xiaokun LiOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health) & School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China. xiaokunli@wmu.edu.cn.ORCID 0000-0002-6556-6262
Pingping ShenState Key Laboratory of Pharmaceutical Biotechnology, Department of Rheumatology and Immunology, The Affiliated Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, School of Life Sciences, Nanjing University, Nanjing, 210023, China. ppshen@nju.edu.cn.ORCID 0000-0002-1072-784X
Nanjing Drum Tower Hospital · CNPeking University · CNWenzhou Medical University · CNChinese Academy of Sciences · CNShenzhen University · CNUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Beige adipocytes in mammalian white adipose tissue (WAT) can reinforce fat catabolism and energy expenditure. Promoting beige adipocyte biogenesis is a tantalizing tactic for combating obesity and its associated metabolic disorders. Here, we report that a previously unidentified phosphorylation pattern (Thr166) in the DNA-binding domain of PPARγ regulates the inducibility of beige adipocytes. This unique posttranslational modification (PTM) pattern influences allosteric communication between PPARγ and DNA or coactivators, which impedes the PPARγ-mediated transactivation of beige cell-related gene expression in WAT. The genetic mutation mimicking T166 phosphorylation (p-T166) hinders the inducibility of beige adipocytes. In contrast, genetic or chemical intervention in this PTM pattern favors beige cell formation. Moreover, inhibition of p-T166 attenuates metabolic dysfunction in obese mice. Our results uncover a mechanism involved in beige cell fate determination. Moreover, our discoveries provide a promising strategy for guiding the development of novel PPARγ agonists for the treatment of obesity and related metabolic disorders.

Indexed as

Adipocytes, BeigeAdipose Tissue, WhiteAnimalsMammalsMiceObesityPhosphorylationPPAR gammaPPAR gamma

Identifiers

PMID36329235
PMCPMC9984430
OpenAlexW4308294033

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.