Elisa Laaksamo

TL;DR: The aberrant flow conditions caused by sIA geometry are the likely cause of the endothelial dysfunction, which results in accumulation of cytotoxic and pro-inflammatory substances into the sIA wall, as well as thrombus formation.

TL;DR: The results suggest that JNK activity and expression are involved in IA growth and possibly rupture and p38 expression in IAgrowth, and pharmacological therapy affecting the stress-activated mitogen-activated protein kinases, JNK and p 38, may enhance the repair of the IA wall in the future.

TL;DR: The results show that programmed cell death is activated in the IA wall via the intrinsic pathway, and high oxidative stress inThe IA wall is probably a significant cause of the intrinsic activation of cell death.

TL;DR: The signaling pathway profile (apoptosis, cell proliferation, stress signaling) differs between ruptured and unruptured IAs and is associated with IA geometry.

TL;DR: This is the first documented successful culture of SMCs from human IAs, and an access to living human cells of aneurysmal origin gives a new tool in the research of the formation, growth, and rupture of IAs.