NF-kB activation in intracranial aneurysm formation and early growth

被引:1
|
作者
Kumar, Vivig Shantha [1 ]
Resheek, Nerella [2 ]
Kumar, Vignarth Shantha [1 ]
机构
[1] Calif Inst Behav Neurosci & Psychol, Internal Med, Fairfield, CA 94534 USA
[2] Univ Illinois, Coll Med, Gen Surg, Peoria, IL USA
关键词
aneurysmal growth; atherogenesis; cerebral aneurysms; endothelial dysfunction; hemodynamics; NF-kB Activation; vessel inflammation; vessel wall remodeling; INDUCED CEREBRAL ANEURYSMS; NECROSIS-FACTOR-ALPHA; FACTOR-KAPPA-B; ENDOTHELIAL-CELLS; TRANSCRIPTION FACTOR; SHEAR-STRESS; GENE-EXPRESSION; MATRIX METALLOPROTEINASE-2; INFLAMMATORY RESPONSE; MOLECULAR-MECHANISMS;
D O I
10.2217/fnl-2023-0014
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
In recent decades, understanding the molecular mechanisms leading to cerebral aneurysm development has been limited. Advances in molecular biology now suggest a plausible explanation, rooted in a chronically unbalanced high hemodynamic environment. Molecular evidence from human and animal intracranial aneurysm specimens indicates a common pathway, where hemodynamic stresses on the endothelium play a pivotal role. This results in endothelial dysfunction, initiating a cascade of inflammatory vessel wall remodeling and degenerative changes. Notably, Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B), activated in response to turbulent flow, upregulates inflammation-related genes, contributing to aneurysm formation. Further elucidation of NF-kappa B's role in hemodynamic stress-induced upregulation and its impact on structural remodeling holds potential for understanding and addressing cerebral aneurysm formation and progression.
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页数:17
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