Evidence map›Paper›PMID 29748423›Full record

ArticleStroke2018

Role of Myeloid Lineage Cell Autophagy in Ischemic Brain Injury.

Masakazu Kotoda, Hajime Furukawa, Takeshi Miyamoto, Masaaki Korai, Fumiaki Shikata, Atsushi Kuwabara, Xiaoxing Xiong, Caleb Rutledge, Rona G Giffard, Tomoki Hashimoto

Abstract read
In one paragraph

Article in Stroke, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  7. A nexus of lipid andFrontiers in endocrinology · 2022
    Review
  8. 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

10 authors at 2 institutions in 1 country.

Masakazu KotodaFrom the Departments of Anesthesia and Perioperative Care (M.K., H.F., T.M., M.K., F.S., A.K., T.H.).
Hajime FurukawaFrom the Departments of Anesthesia and Perioperative Care (M.K., H.F., T.M., M.K., F.S., A.K., T.H.).
Takeshi MiyamotoFrom the Departments of Anesthesia and Perioperative Care (M.K., H.F., T.M., M.K., F.S., A.K., T.H.).
Masaaki KoraiFrom the Departments of Anesthesia and Perioperative Care (M.K., H.F., T.M., M.K., F.S., A.K., T.H.).
Fumiaki ShikataFrom the Departments of Anesthesia and Perioperative Care (M.K., H.F., T.M., M.K., F.S., A.K., T.H.).
Atsushi KuwabaraFrom the Departments of Anesthesia and Perioperative Care (M.K., H.F., T.M., M.K., F.S., A.K., T.H.).
Xiaoxing XiongDepartment of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, CA (X.X., R.G.G.).
Caleb RutledgeNeurological Surgery (C.R., T.H.), University of California, San Francisco.
Rona G GiffardDepartment of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, CA (X.X., R.G.G.).
Tomoki HashimotoFrom the Departments of Anesthesia and Perioperative Care (M.K., H.F., T.M., M.K., F.S., A.K., T.H.) tomoki.hashimoto@barrowneuro.org.
Neurological Surgery · USStanford University · US

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
Stress Proteins in Brain Cell InjuryR01NS084396 · NINDS · STANFORD UNIVERSITY · PI GIFFARD, RONA G · 2013 to 2017
$1.7M
Mitochondrial protection in post-stroke recoveryR01NS080177 · NINDS · STANFORD UNIVERSITY · PI GIFFARD, RONA G · 2013 to 2017
$1.7M
NINDS NIH HHS R01 NS055876NINDS NIH HHS R01 NS080177NINDS NIH HHS R01 NS082280NINDS NIH HHS R01 NS084396
6 · The paper itself

Abstract

background and purposeInflammatory cells play a significant role in secondary injury after ischemic stroke. Recent studies have suggested that a lack of autophagy in myeloid cells causes augmented proinflammatory cytokine release and prolonged inflammation after tissue injury. In this study, we investigated the roles of myeloid cell autophagy in ischemic brain injury.

methodsFocal cerebral ischemia was induced via transient middle cerebral artery occlusion in mice with autophagy-deficient myeloid lineage cells (Atg5flox/flox LysMCre+) and in their littermate controls (Atg5flox/flox). Infarct volume, neurological function, inflammatory cell infiltration, and proinflammatory cytokine expression levels were evaluated.

resultsMice lacking autophagy in myeloid lineage cells had a lower survival rate for 14 days than control mice (20% versus 70%;

conclusionsThese data suggest that the lack of myeloid cell autophagy aggravates secondary injury by augmenting and prolonging inflammation after ischemic stroke without affecting the initial injury.

Indexed as

AnimalsAutophagyBrainBrain InjuriesBrain IschemiaCell LineageCytokinesDisease Models, AnimalInfarction, Middle Cerebral ArteryInflammationMice, TransgenicMyeloid CellsStrokeCytokinesautophagybrain ischemiainflammationmyeloid cellsstroke

Identifiers

PMID29748423
PMCPMC5970995
OpenAlexW2801267769

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.