| Autor: |
Blaj LA; Department of Neurosurgery, 'Grigore T. Popa' University of Medicine and Pharmacy, 700115 Iasi, Romania.; 'Prof. Dr. N. Oblu' Emergency Clinical Hospital, 700309 Iasi, Romania., Cucu AI; 'Prof. Dr. N. Oblu' Emergency Clinical Hospital, 700309 Iasi, Romania.; Faculty of Medicine and Biological Sciences, University Stefan cel Mare of Suceava, 720229 Suceava, Romania., Tamba BI; Advanced Research and Development Center for Experimental Medicine (CEMEX), 'Grigore T. Popa' University of Medicine and Pharmacy, 700115 Iasi, Romania.; Department of Pharmacology, Clinical Pharmacology and Algesiology, 'Grigore T. Popa' University of Medicine and Pharmacy, 700115 Iasi, Romania., Turliuc MD; Department of Neurosurgery, 'Grigore T. Popa' University of Medicine and Pharmacy, 700115 Iasi, Romania.; 'Prof. Dr. N. Oblu' Emergency Clinical Hospital, 700309 Iasi, Romania. |
| Abstrakt: |
The pathophysiology of intracranial aneurysms (IA) has been proven to be closely linked to hemodynamic stress and inflammatory pathways, most notably the NF-kB pathway. Therefore, it is a potential target for therapeutic intervention. In the present review, we investigated alterations in the vascular smooth muscle cells (VSMCs), extracellular matrix, and endothelial cells by the mediators implicated in the NF-kB pathway that lead to the formation, growth, and rupture of IAs. We also present an overview of the NF-kB pathway, focusing on stimuli and transcriptional targets specific to IAs, as well as a summary of the current strategies for inhibiting NF-kB activation in IAs. Our report adds to previously reported data and future research directions for treating IAs using compounds that can suppress inflammation in the vascular wall. |
