Evidence map›Paper›PMID 32788447›Full record

ArticleNeural regeneration research2021

The NLRP3 inflammasome: a potential therapeutic target for traumatic brain injury.

Saifudeen Ismael, Heba A Ahmed, Tusita Adris, Kehkashan Parveen, Parth Thakor, Tauheed Ishrat

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neural regeneration research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 73 citations in OpenAlex.

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  5. Intraparenchymal B cell therapy protects neurological function and modulates local neuroinflammation in experimental hemorrhagic stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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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

6 authors at 2 institutions in 2 countries.

Saifudeen IsmaelDepartment of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, TN, USA.
Heba A AhmedDepartment of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, TN, USA.
Tusita AdrisDepartment of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, TN, USA.
Kehkashan ParveenDepartment of Biochemistry, Hamdard University, New Delhi, India.
Parth ThakorDepartment of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, TN, USA.
Tauheed IshratDepartment of Anatomy and Neurobiology; Neuroscience Institute, University of Tennessee Health Science Center, Memphis, TN, USA.
University of Tennessee Health Science Center · USJamia Hamdard · IN

Funding

Mechanisms and therapeutic targets of neurovascular injury in hyperglycemic strokeR01NS097800 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI ISHRAT, TAUHEED · 2016 to 2020
$1.6M
NINDS NIH HHS R01 NS097800
6 · The paper itself

Abstract

Although the precise mechanisms contributing to secondary brain injury following traumatic brain injury are complex and obscure, a number of studies have demonstrated that inflammatory responses are an obvious and early feature in the pathogenesis of traumatic brain injury. Inflammasomes are multiprotein complexes that prompt the stimulation of caspase-1 and subsequently induce the maturation and secretion of proinflammatory cytokines, such as interleukin-1β and interleukin-18. These cytokines play a pivotal role in facilitating innate immune responses and inflammation. Among various inflammasome complexes, the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is the best characterized, a crucial role for NLRP3 has been demonstrated in various brain diseases, including traumatic brain injury. Several recent studies have revealed the contribution of NLRP3 inflammasome in identifying cellular damage and stimulating inflammatory responses to aseptic tissue injury after traumatic brain injury. Even more important, blocking or inhibiting the activation of the NLRP3 inflammasome may have substantial potential to salvage tissue damage during traumatic brain injury. In this review, we summarize recently described mechanisms that are involved in the activation and regulation of the NLRP3 inflammasome. Moreover, we review the recent investigations on the contribution of the NLRP3 inflammasome in the pathophysiology of TBI, and current advances and challenges in potential NLRP3-targeted therapies. A significant contribution of NLRP3 inflammasome activation to traumatic brain injury implies that therapeutic approaches focused on targeting specific inflammasome components could significantly improve the traumatic brain injury outcomes.

Indexed as

caspase-1inflammationinterleukin-1βMCC950NLRP3-inflammasometraumatic brain injury

Identifiers

PMID32788447
PMCPMC7818859
OpenAlexW3048712936

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.