Regulation of <scp>BzATP</scp>‐Induced Blood–Brain Barrier Endothelial Cell Hyperpermeability by <scp>NLRP3</scp> Inflammasome Inhibition

NLRP3 inflammasome signaling is critical to BBB endothelial cell dysfunction. Extracellular ATP is an upstream promoter of BBB hyperpermeability. NLRP3 inflammasome activation leads to subsequent caspase-1 and MMP-9-mediated tight junction protein disarray.

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Publication Details

Journal
Microcirculation
Published
2025-03-07
DOI
https://doi.org/10.1111/micc.70006
Citations
3
Primary Topic
Barrier Structure and Function Studies
Type
article
Field-Weighted Citation Impact
2.53

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article

Regulation of BzATP‐Induced Blood–Brain Barrier Endothelial Cell Hyperpermeability by NLRP3 Inflammasome Inhibition

Amrendra K. Singh, O’lisa Yaa Waithe, Binu Tharakan, Gabriela Seplovich et al.
3 citations
Microcirculation
Barrier Structure and Function Studies
2.53
article

Regulation of BzATP‐Induced Blood–Brain Barrier Endothelial Cell Hyperpermeability by NLRP3 Inflammasome Inhibition

Amrendra K. Singh, O’lisa Yaa Waithe, Binu Tharakan, Gabriela Seplovich, Aliyah Anderson, Chris Greene, Saravanakumar Muthusamy, Oluwatoyin Olagunju
article en
3 citations

Abstract

NLRP3 inflammasome signaling is critical to BBB endothelial cell dysfunction. Extracellular ATP is an upstream promoter of BBB hyperpermeability. NLRP3 inflammasome activation leads to subsequent caspase-1 and MMP-9-mediated tight junction protein disarray.

MicrocirculationVol. 32(3)
Morehouse School of Medicine (US)
National Institutes of Health, National Institute of Neurological Disorders and Stroke
Good health and well-being
Openalex Percentile: Top 12%
Barrier Structure and Function Studies
2.53
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