Evidence map›Paper›PMID 34268418›Full record

ArticleAnnals of translational medicine2021

Irisin ameliorates nicotine-mediated atherosclerosis via inhibition of the PI3K pathway.

Kang Li, Junye Chen, Chaonan Wang, Jiang Shao, Zhichao Lai, Xiaoxi Yu, Fenghe Du, Ran Gao, Jing Wang, Bao Liu

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Role of irisin in physiology and pathology.Frontiers in endocrinology · 2022
    Review
  6. Article
  7. 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

10 authors at 2 institutions in 1 country.

Kang LiDepartment of Vascular Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, China.
Junye ChenDepartment of Vascular Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, China.
Chaonan WangDepartment of Vascular Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, China.
Jiang ShaoDepartment of Vascular Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, China.
Zhichao LaiDepartment of Vascular Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, China.
Xiaoxi YuDepartment of Vascular Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, China.
Fenghe DuDepartment of Vascular Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, China.
Ran GaoState Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Department of Pathophysiology, Peking Union Medical College, Beijing, China.
Jing WangState Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Department of Pathophysiology, Peking Union Medical College, Beijing, China.
Bao LiuDepartment of Vascular Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, China.
Peking Union Medical College Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtherosclerosis is a chronic disease, with smoking being an independent risk factor. Irisin, a factor produced by myocytes, is expected to treat smoking-related arteriosclerosis, however its specific mechanism remains unclear.

methodsForty

resultsH&E staining and Masson staining showed that nicotine could aggravate the intensity of atherosclerosis in mice, and Irisin could reverse the thickening of the vascular media induced by nicotine. Immunohistochemical staining of CD68 and α-SMA suggested that Irisin could inhibit nicotine-mediated macrophage infiltration and smooth muscle cell proliferation. The protective effect of Irisin was partially reduced after the administration of cilengitide, confirming that Irisin enters cells through multiple ways, including integrin αvβ5. Nicotine was confirmed to activate the PI3K pathway to promote media thickening, while Irisin can inhibit the activation of the PI3K pathway, thus playing its anti-atherosclerosis role. Irisin was further observed to reverse nicotine-mediated P27 down-regulation.

conclusionsIrisin was found to inhibit nicotine-mediated medium thickening, smooth muscle cell proliferation, macrophage infiltration, and atherosclerosis progression via the integrin αVβ5/PI3K/P27 pathway.

Indexed as

atherosclerosisintegrin αVβ5IrisinnicotinePI3K

Identifiers

PMID34268418
PMCPMC8246167
OpenAlexW3160757321

What OpenQuestion holds

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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.