Evidence map›Paper›PMID 25931465›Full record

ArticleStroke2015

Protective Role of Peroxisome Proliferator-Activated Receptor-γ in the Development of Intracranial Aneurysm Rupture.

Kenji Shimada, Hajime Furukawa, Kosuke Wada, Masaaki Korai, Yuan Wei, Yoshiteru Tada, Atsushi Kuwabara, Fumiaki Shikata, Keiko T Kitazato, Shinji Nagahiro and 2 more

Open access · greenAbstract read
In one paragraph

Article in Stroke, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 2 pooled it
3.8field-weighted citation impact, top 7% 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

54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Vitamin D deficiency promotes intracranial aneurysm rupture.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. A Future Blood Test to Detect Cerebral Aneurysms.Cellular and molecular neurobiology · 2023
    Review
  14. Integrative analysis of multi-omics data to identify three immune-related genes in the formation and progression of intracranial aneurysms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  15. Review
  16. Article
  17. Review
  18. Understanding the genetics of intracranial aneurysms: A primer.Clinical neurology and neurosurgery · 2022
    Review
  19. Article
  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

12 authors at 1 institution in 2 countries.

Kenji ShimadaFrom the Departments of Anesthesia and Perioperative Care (K.S., H.F., K.W., M.K., Y.W., A.K., F.S., T.H.) and Neurological Surgery (M.T.L.), University of California, San Francisco; and Department of Neurosurgery (K.S., M.K., Y.T., K.T.K., S.N.), School of Medicine, The University of Tokushima, Tokushima City, Japan.
Hajime FurukawaFrom the Departments of Anesthesia and Perioperative Care (K.S., H.F., K.W., M.K., Y.W., A.K., F.S., T.H.) and Neurological Surgery (M.T.L.), University of California, San Francisco; and Department of Neurosurgery (K.S., M.K., Y.T., K.T.K., S.N.), School of Medicine, The University of Tokushima, Tokushima City, Japan.
Kosuke WadaFrom the Departments of Anesthesia and Perioperative Care (K.S., H.F., K.W., M.K., Y.W., A.K., F.S., T.H.) and Neurological Surgery (M.T.L.), University of California, San Francisco; and Department of Neurosurgery (K.S., M.K., Y.T., K.T.K., S.N.), School of Medicine, The University of Tokushima, Tokushima City, Japan.
Masaaki KoraiFrom the Departments of Anesthesia and Perioperative Care (K.S., H.F., K.W., M.K., Y.W., A.K., F.S., T.H.) and Neurological Surgery (M.T.L.), University of California, San Francisco; and Department of Neurosurgery (K.S., M.K., Y.T., K.T.K., S.N.), School of Medicine, The University of Tokushima, Tokushima City, Japan.
Yuan WeiFrom the Departments of Anesthesia and Perioperative Care (K.S., H.F., K.W., M.K., Y.W., A.K., F.S., T.H.) and Neurological Surgery (M.T.L.), University of California, San Francisco; and Department of Neurosurgery (K.S., M.K., Y.T., K.T.K., S.N.), School of Medicine, The University of Tokushima, Tokushima City, Japan.
Yoshiteru TadaFrom the Departments of Anesthesia and Perioperative Care (K.S., H.F., K.W., M.K., Y.W., A.K., F.S., T.H.) and Neurological Surgery (M.T.L.), University of California, San Francisco; and Department of Neurosurgery (K.S., M.K., Y.T., K.T.K., S.N.), School of Medicine, The University of Tokushima, Tokushima City, Japan.
Atsushi KuwabaraFrom the Departments of Anesthesia and Perioperative Care (K.S., H.F., K.W., M.K., Y.W., A.K., F.S., T.H.) and Neurological Surgery (M.T.L.), University of California, San Francisco; and Department of Neurosurgery (K.S., M.K., Y.T., K.T.K., S.N.), School of Medicine, The University of Tokushima, Tokushima City, Japan.
Fumiaki ShikataFrom the Departments of Anesthesia and Perioperative Care (K.S., H.F., K.W., M.K., Y.W., A.K., F.S., T.H.) and Neurological Surgery (M.T.L.), University of California, San Francisco; and Department of Neurosurgery (K.S., M.K., Y.T., K.T.K., S.N.), School of Medicine, The University of Tokushima, Tokushima City, Japan.
Keiko T KitazatoFrom the Departments of Anesthesia and Perioperative Care (K.S., H.F., K.W., M.K., Y.W., A.K., F.S., T.H.) and Neurological Surgery (M.T.L.), University of California, San Francisco; and Department of Neurosurgery (K.S., M.K., Y.T., K.T.K., S.N.), School of Medicine, The University of Tokushima, Tokushima City, Japan.
Shinji NagahiroFrom the Departments of Anesthesia and Perioperative Care (K.S., H.F., K.W., M.K., Y.W., A.K., F.S., T.H.) and Neurological Surgery (M.T.L.), University of California, San Francisco; and Department of Neurosurgery (K.S., M.K., Y.T., K.T.K., S.N.), School of Medicine, The University of Tokushima, Tokushima City, Japan.
Michael T LawtonFrom the Departments of Anesthesia and Perioperative Care (K.S., H.F., K.W., M.K., Y.W., A.K., F.S., T.H.) and Neurological Surgery (M.T.L.), University of California, San Francisco; and Department of Neurosurgery (K.S., M.K., Y.T., K.T.K., S.N.), School of Medicine, The University of Tokushima, Tokushima City, Japan.
Tomoki HashimotoFrom the Departments of Anesthesia and Perioperative Care (K.S., H.F., K.W., M.K., Y.W., A.K., F.S., T.H.) and Neurological Surgery (M.T.L.), University of California, San Francisco; and Department of Neurosurgery (K.S., M.K., Y.T., K.T.K., S.N.), School of Medicine, The University of Tokushima, Tokushima City, Japan. hashimot@anesthesia.ucsf.edu.
Norwegian Womens Public Health Association · NO

Funding

Intracranial Aneurysm Pathogenesis-Roles of Vascular Remodeling and InflammationR01NS055876 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HASHIMOTO, TOMOKI · 2007 to 2015
$3.0M
The Role of Mast Cells in the Pathophysiology of Intracranial AneurysmR01NS082280 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HASHIMOTO, TOMOKI · 2013 to 2017
$1.7M
NINDS NIH HHS R01 NS055876NINDS NIH HHS R01NS055876NINDS NIH HHS R01 NS082280NINDS NIH HHS R01NS082280
6 · The paper itself

Abstract

background and purposeInflammation is emerging as a key component of the pathophysiology of intracranial aneurysms. Peroxisome proliferator-activated receptor-γ (PPARγ) is a nuclear hormone receptor of which activation modulates various aspects of inflammation.

methodsUsing a mouse model of intracranial aneurysm, we examined the potential roles of PPARγ in the development of rupture of intracranial aneurysm.

resultsA PPARγ agonist, pioglitazone, significantly reduced the incidence of ruptured aneurysms and the rupture rate without affecting the total incidence aneurysm (unruptured aneurysms and ruptured aneurysms). PPARγ antagonist (GW9662) abolished the protective effect of pioglitazone. The protective effect of pioglitazone was absent in mice lacking macrophage PPARγ. Pioglitazone treatment reduced the mRNA levels of inflammatory cytokines (monocyte chemoattractant factor-1, interleukin-1, and interleukin-6) that are primarily produced by macrophages in the cerebral arteries. Pioglitazone treatment reduced the infiltration of M1 macrophage into the cerebral arteries and the macrophage M1/M2 ratio. Depletion of macrophages significantly reduced the rupture rate.

conclusionsOur data showed that the activation of macrophage PPARγ protects against the development of aneurysmal rupture. PPARγ in inflammatory cells may be a potential therapeutic target for the prevention of aneurysmal rupture.

Indexed as

Aneurysm, RupturedAnilidesAnimalsCerebral ArteriesCytokinesHypoglycemic AgentsIntracranial AneurysmMacrophagesMiceMice, KnockoutPioglitazonePPAR gammaThiazolidinediones2-chloro-5-nitrobenzanilideAnilidesCytokinesHypoglycemic AgentsPioglitazonePPAR gammaThiazolidinedionesinflammationintracranial aneurysmsubarachnoid hemorrhage

Identifiers

PMID25931465
PMCPMC4447500
OpenAlexW1971120195

What OpenQuestion holds

Textmetadata
LicenceTDM
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.