Evidence map›Paper›PMID 33919485›Full record

SynthesisInternational journal of molecular sciences2021

Role of Adaptor Protein Myeloid Differentiation 88 (MyD88) in Post-Subarachnoid Hemorrhage Inflammation: A Systematic Review.

Hammad Ahmed, Mahtab Ahmad Khan, Ulf Dietrich Kahlert, Mika Niemelä, Daniel Hänggi, Shafqat Rasul Chaudhry, Sajjad Muhammad

Open access · goldAbstract readSystematic Review
In one paragraph

Synthesis in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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  13. Pharmacological targeting of adaptor proteins in chronic inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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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

7 authors at 5 institutions in 3 countries.

Hammad AhmedDepartment of Basic Medical Sciences, Imran Idrees College of Pharmacy, University of the Punjab, Sialkot 51310, Pakistan.
Mahtab Ahmad KhanDepartment of Pharmacology, Faculty of Pharmacy, University of Central Punjab (UCP), Lahore 54000, Pakistan.ORCID 0000-0001-5703-2730
Ulf Dietrich KahlertDepartment of Neurosurgery, Medical Faculty, Heinrich-Heine University of Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0000-0002-6021-1841
Mika NiemeläDepartment of Neurosurgery, University of Helsinki and University Hospital, FI-00029 HUS Helsinki, Finland.
Daniel HänggiDepartment of Neurosurgery, Medical Faculty, Heinrich-Heine University of Düsseldorf, 40225 Düsseldorf, Germany.
Shafqat Rasul ChaudhryDepartment of Basic Medical Sciences, Shifa College of Pharmaceutical Sciences, Shifa Tameer-e-Millat University, Islamabad 44000, Pakistan.
Sajjad MuhammadDepartment of Neurosurgery, Medical Faculty, Heinrich-Heine University of Düsseldorf, 40225 Düsseldorf, Germany.
Heinrich Heine University Düsseldorf · DEUniversity of Helsinki · FIShifa Tameer-e-Millat University · PKUniversity of Central Punjab · PKUniversity of the Punjab · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid differentiation 88 (MyD88) is a well-established inflammatory adaptor protein. It is one of the essential downstream proteins of the toll-like receptor 4 (TLR4) signaling pathway. TLRs are pattern recognition receptors that are usually activated by the damage-associated molecular pattern molecules (DAMPs). Sterile inflammation is triggered by the endogenous DAMPs released in response to global cerebral ischemia and from extravasated blood after subarachnoid hemorrhage (SAH). In this review, we highlight the importance of the neuroinflammatory role of the MyD88 in the SAH. We also explore a few possible pharmacological agents that can be used to decrease SAH-associated neuroinflammation by modulating the MyD88 dependent functions. Pharmacological agents such as flavonoids, melatonin, fluoxetine, pentoxifylline and progesterone have been investigated experimentally to reduce the SAH-associated inflammation. Inhibition of the MyD88 not only reduces the expression of pro-inflammatory cytokines, but also potentially inhibits other processes that can augment the SAH associated inflammation. Further investigations are required to translate these findings in the clinical setting.

Indexed as

AnimalsHumansInflammationMyeloid Differentiation Factor 88Receptors, Pattern RecognitionSubarachnoid HemorrhageMyeloid Differentiation Factor 88Receptors, Pattern Recognitionaneurysmsneuro-inflammationpattern recognition receptorspost-SAH complicationsstroke

Identifiers

PMID33919485
PMCPMC8073517
OpenAlexW3152695453

What OpenQuestion holds

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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.