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Arterial dilation can lead to aneurysm formation, most commonly affecting the aorta and intracranial arteries. Platelets are now recognized as key mediators of vascular inflammation and remodeling, contributing to the initiation and progression of several vascular diseases. While the role of platelets in abdominal aortic aneurysm formation has gained considerable attention and is under active investigation, their contribution to intracranial aneurysm pathophysiology remains poorly understood. In this review, we summarize current mechanistic and preclinical evidence on the development and rupture of intracranial aneurysms. We discuss how platelet interactions with leukocytes, vascular cells, and their procoagulant role may influence inflammatory and tissue damage within the intracranial aneurysm, highlighting gaps in knowledge that could reveal new mechanisms.
Maupu et al. (Thu,) studied this question.