Evidence map›Paper›PMID 29233981›Full record

ArticleNature communications2017

A miR-327-FGF10-FGFR2-mediated autocrine signaling mechanism controls white fat browning.

Carina Fischer, Takahiro Seki, Sharon Lim, Masaki Nakamura, Patrik Andersson, Yunlong Yang, Jennifer Honek, Yangang Wang, Yanyan Gao, Fang Chen and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. FGF-based drug discovery: advances and challenges.Nature reviews. Drug discovery · 2025
    Review
  3. Review
  4. Review
  5. Article
  6. Pulling the trigger: Noncoding RNAs in white adipose tissue browning.Reviews in endocrine & metabolic disorders · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Time of day determines postexercise metabolism in mouse adipose tissue.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
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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

19 authors at 7 institutions in 4 countries.

Carina FischerDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institute, 171 77, Stockholm, Sweden.
Takahiro SekiDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institute, 171 77, Stockholm, Sweden.
Sharon LimDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institute, 171 77, Stockholm, Sweden.
Masaki NakamuraDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institute, 171 77, Stockholm, Sweden.
Patrik AnderssonDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institute, 171 77, Stockholm, Sweden.
Yunlong YangDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institute, 171 77, Stockholm, Sweden.
Jennifer HonekDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institute, 171 77, Stockholm, Sweden.
Yangang WangDepartment of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao, 266003, China.
Yanyan GaoDepartment of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao, 266003, China.
Fang ChenHospital of Zhejiang Chinese Medicine University, 54 Youdian Road, Hangzhou, Zhejiang, 310006, China.
Nilesh J SamaniDepartment of Cardiovascular Sciences, University of Leicester and NIHR Leicester Cardiovascular Biomedical Research Unit, Glenfield Hospital, Leicester, LE3 9QP, UK.
Jun ZhangDivision of Molecular Biology, Institute for Genome Research, Institute of Advanced Medical Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima, 770-8503, Japan.
Masato MiyakeDivision of Molecular Biology, Institute for Genome Research, Institute of Advanced Medical Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima, 770-8503, Japan.
Seiichi OyadomariDivision of Molecular Biology, Institute for Genome Research, Institute of Advanced Medical Sciences, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima, 770-8503, Japan.
Akihiro YasueDepartment of Orthodontics Dentofacial Orthopedics, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima, 770-8504, Japan.
Xuri LiState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, 510060, China.
Yun ZhangThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Shandong University Qilu Hospital, Jinan, Shandong, 250012, China.
Yizhi LiuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, 510060, China.
Yihai CaoDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institute, 171 77, Stockholm, Sweden. yihai.cao@ki.se.
Karolinska Institutet · SETokushima University · JPQilu Hospital of Shandong University · CNQingdao University · CNSun Yat-sen University · CNNIHR Leicester Cardiovascular Biomedical Research Unit · GBZhejiang Chinese Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding the molecular mechanisms regulating beige adipocyte formation may lead to the development of new therapies to combat obesity. Here, we report a miRNA-based autocrine regulatory pathway that controls differentiation of preadipocytes into beige adipocytes. We identify miR-327 as one of the most downregulated miRNAs targeting growth factors in the stromal-vascular fraction (SVF) under conditions that promote white adipose tissue (WAT) browning in mice. Gain- and loss-of-function experiments reveal that miR-327 targets FGF10 to prevent beige adipocyte differentiation. Pharmacological and physiological β-adrenergic stimulation upregulates FGF10 levels and promotes preadipocyte differentiation into beige adipocytes. In vivo local delivery of miR-327 to WATs significantly compromises the beige phenotype and thermogenesis. Contrarily, systemic inhibition of miR-327 in mice induces browning and increases whole-body metabolic rate under thermoneutral conditions. Our data provide mechanistic insight into an autocrine regulatory signaling loop that regulates beige adipocyte formation and suggests that the miR-327-FGF10-FGFR2 signaling axis may be a therapeutic targets for treatment of obesity and metabolic diseases.

Indexed as

AdipocytesAdipose Tissue, BeigeAdipose Tissue, WhiteAnimalsAutocrine CommunicationCell DifferentiationDiabetes Mellitus, Type 2Down-RegulationEnergy MetabolismFemaleFibroblast Growth Factor 10MiceMice, Inbred C57BLMice, Inbred NODMicroRNAsModels, AnimalFgf10 protein, mouseFgfr2 protein, mouseFibroblast Growth Factor 10MicroRNAsMIRN327 microRNA, mouseReceptor, Fibroblast Growth Factor, Type 2RNA, Small Interfering

Identifiers

PMID29233981
PMCPMC5727036
OpenAlexW2772017853

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.