Evidence map›Paper›PMID 39803918›Full record

ArticleAdipocyte2025

Anti-inflammatory effect of Angiotensin 1-7 in white adipose tissue.

Nozomi Nishida, Satoru Sugimoto, Satoshi Miyagaki, Chiharu Cho, Madoka Konishi, Takeshi Goda, Mihoko Yamaguchi, Yasuhiro Kawabe, Hidechika Morimoto, Joji Kusuyama and 6 more

Abstract read
In one paragraph

Article in Adipocyte, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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.

Nozomi NishidaDepartment of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Satoru SugimotoDepartment of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.ORCID 0000-0002-2691-3399
Satoshi MiyagakiDepartment of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Chiharu ChoDepartment of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Madoka KonishiDepartment of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Takeshi GodaDepartment of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Mihoko YamaguchiDepartment of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Yasuhiro KawabeDepartment of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Hidechika MorimotoDepartment of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Joji KusuyamaDepartment of Biosignals and Inheritance, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan.
Takuro OkamuraDepartment of Endocrinology and Metabolism, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Masahide HamaguchiDepartment of Endocrinology and Metabolism, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Jun MoriDivision of Pediatric Endocrinology, Metabolism and Nephrology, Children's Medical Center, Osaka City General Hospital, Osaka, Japan.
Hisakazu NakajimaDepartment of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Michiaki FukuiDepartment of Endocrinology and Metabolism, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Tomoko IeharaDepartment of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity is a global health concern that promotes chronic low-grade inflammation, leading to insulin resistance, a key factor in many metabolic diseases. Angiotensin 1-7 (Ang 1-7), a component of the renin-angiotensin system (RAS), exhibits anti-inflammatory effects in obesity and related disorders, though its mechanisms remain unclear. In this study, we examined the effect of Ang 1-7 on inflammation of white adipose tissue (WAT) in dietary-induced obese mice. Monocyte chemoattractant protein-1 (MCP-1) produced by white adipocytes and tumour necrosis factor-α (TNF-α) produced by macrophages are pro-inflammatory cytokines and interact to form a pathogenic loop to exacerbate obesity-induced inflammation. We found that Ang 1-7 reduced MCP-1 and TNF-α gene expressions and the number of crown-like structures, which are histological hallmarks of the pro-inflammatory process, in visceral epididymal WAT (eWAT) and reduced circulating MCP-1 and TNF-α levels, accompanied by improvement in insulin resistance, in dietary-induced obese mice. Furthermore, Ang 1-7 reduced MCP-1 and TNF-α secretions in 3T3-L1 white adipocytes and RAW 264.7 macrophages, respectively, which are

Indexed as

Adipose Tissue, WhiteAngiotensin IAnti-Inflammatory AgentsPeptide Fragments3T3-L1 CellsAnimalsChemokine CCL2InflammationInsulin ResistanceMacrophagesMaleMiceMice, Inbred C57BLObesityRAW 264.7 CellsTumor Necrosis Factor-alphaAngiotensin Iangiotensin I (1-7)Anti-Inflammatory AgentsCcl2 protein, mouseChemokine CCL2Peptide FragmentsTumor Necrosis Factor-alphaAngiotensin 1-7anti-inflammatory effectMCP-1obesityTNF-α

Identifiers

PMID39803918
PMCPMC11730366

What Socratic 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 Socratic graph.