NF-kB activation in intracranial aneurysm formation and early growth

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.