Evidence map›Paper›PMID 31468571›Full record

ReviewJournal of neuroscience research2020

The role of TLR4 and HO-1 in neuroinflammation after subarachnoid hemorrhage.

Yosuke Akamatsu, Vicente A Pagan, Khalid A Hanafy

Open access · greenAbstract readReview
In one paragraph

Review in Journal of neuroscience research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Toll like receptor 4 (TLR4) in neuroinflammation: From acute hemorrhagic stroke to chronic neurodegeneration.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Role of microglia after subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Review
  8. Review
  9. Immunological Profile of Vasospasm after Subarachnoid Hemorrhage.International journal of molecular sciences · 2023
    Review
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  11. Article
  12. Article
  13. Review
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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

3 authors at 1 institution in 1 country.

Yosuke AkamatsuDepartment of Surgery, Division of Neurosurgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Vicente A PaganDepartment of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Khalid A HanafyDepartment of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.ORCID 0000-0002-5979-1367
Beth Israel Deaconess Medical Center · US

Funding

Modulation of the TLR4-Lyn interaction in SAHR01NS109174 · NINDS · ROWAN UNIVERSITY · PI HANAFY, KHALID A. · 2019 to 2023
$2.4M
The role of TLR4-dependent sterile inflammation in mediating adverse outcomes after SAHR21NS099606 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI HANAFY, KHALID A. · 2017 to 2018
$476k
American Heart Association #17GRNT33670058NINDS NIH HHS 1R01 NS109174NINDS NIH HHS R01 NS109174NINDS NIH HHS R21 NS099606
6 · The paper itself

Abstract

This review on the mechanisms of neuroinflammation following subarachnoid hemorrhage will focus mainly on toll-like receptor 4 (TLR4), Heme Oxygenase-1 (HO-1), and the role of microglia and macrophages in this process. Vasospasm has long been the focus of research in SAH; however, clinical trials have shown that amelioration of vasospasm does not lead to an improved clinical outcome. This necessitates the need for novel avenues of research. Our work has demonstrated that microglial TLR4 and microglial HO-1, not only affects cognitive dysfunction, but also circadian dysrhythmia in a mouse model of SAH. To attempt to translate these findings, we have also begun investigating macrophages in the cerebrospinal fluid of SAH patients. The goal of this review is to provide an update on the role of TLR4, HO-1, and other signal transduction pathways in SAH-induced neuroinflammation.

Indexed as

AnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenEncephalitisHeme Oxygenase (Decyclizing)HMGB1 ProteinHumansMitogen-Activated Protein KinasesReceptors, Cell SurfaceSignal TransductionSubarachnoid HemorrhageToll-Like Receptor 4Antigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenHeme Oxygenase (Decyclizing)HMGB1 ProteinMitogen-Activated Protein KinasesReceptors, Cell SurfaceToll-Like Receptor 4adaptive immunityCD163Heme-Oxygenaseinnate immunitymicrogliasubarachnoid hemorrhagetoll like receptor

Identifiers

PMID31468571
PMCPMC6980436
OpenAlexW2970225658

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.