Evidence map›Paper›PMID 38100414›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2023

FAP expression in adipose tissue macrophages promotes obesity and metabolic inflammation.

Yunyun Wu, Chao Wu, Tiancong Shi, Qian Cai, Tianyao Wang, Yingluo Xiong, Yubin Zhang, Wei Jiang, Mingfang Lu, Zhengrong Chen and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. FAPαAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article
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

13 authors at 4 institutions in 1 country.

Yunyun Wu *Department of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.ORCID 0009-0006-2296-9439
Chao Wu *Department of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Tiancong ShiDepartment of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Qian CaiDepartment of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Tianyao WangDepartment of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Yingluo XiongDepartment of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.ORCID 0000-0003-3421-2119
Yubin ZhangMinistry of Education Key Laboratory of Public Health, School of Public Health, Fudan University, Shanghai 200032, China.ORCID 0000-0002-7114-3485
Wei JiangDepartment of Rheumatology and Immunology, The Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China.ORCID 0000-0001-7698-3857
Mingfang LuDepartment of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.ORCID 0000-0002-8612-3444
Zhengrong ChenDepartment of Respiratory Diseases, Children's Hospital of Soochow University, Suzhou 215008, China.
Jing ChenDepartment of Nephrology, Huashan hospital, Fudan University, Shanghai 200040, China.
Jiqiu WangDepartment of Endocrinology and Metabolism, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Rui HeDepartment of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.ORCID 0000-0001-5288-9786
Fudan University · CNGuiyang Medical University · CNShanghai Jiao Tong University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipose tissue macrophages (ATM) are key players in the development of obesity and associated metabolic inflammation which contributes to systemic metabolic dysfunction. We here found that fibroblast activation protein α (FAP), a well-known marker of cancer-associated fibroblast, is selectively expressed in murine and human ATM among adipose tissue-infiltrating leukocytes. Macrophage FAP deficiency protects mice against diet-induced obesity and proinflammatory macrophage infiltration in obese adipose tissues, thereby alleviating hepatic steatosis and insulin resistance. Mechanistically, FAP specifically mediates monocyte chemokine protein CCL8 expression by ATM, which is further upregulated upon high-fat-diet (HFD) feeding, contributing to the recruitment of monocyte-derived proinflammatory macrophages with no effect on their classical inflammatory activation. CCL8 overexpression restores HFD-induced metabolic phenotypes in the absence of FAP. Moreover, macrophage FAP deficiency enhances energy expenditure and oxygen consumption preceding differential body weight after HFD feeding. Such enhanced energy expenditure is associated with increased levels of norepinephrine (NE) and lipolysis in white adipose tissues, likely due to decreased expression of monoamine oxidase, a NE degradation enzyme, by

Indexed as

Adipose TissueInsulin ResistanceAnimalsDiet, High-FatFibroblast Activation Protein AlphaHumansInflammationMacrophagesMiceMice, Inbred C57BLObesityFibroblast Activation Protein AlphaCCL8fibroblast activation protein (FAP)inflammationmacrophageobesity

Identifiers

PMID38100414
PMCPMC10743525
OpenAlexW4389779502

What OpenQuestion 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 OpenQuestion graph.