<p>The mechanisms underlying the formation and rupture of intracranial aneurysms remain unclear. Rupture of the aneurysmal wall causes subarachnoid hemorrhage, with a mortality rate of 35–50%. Literature suggests that rupture is associated with the remodeling of the aneurysmal wall, including endothelial cell damage, smooth muscle cells (SMCs) proliferation, and inflammatory cell infiltration, particularly macrophages. Transforming growth factor β (TGF-β) is a multifunctional factor that plays a diverse role in cell growth and differentiation. It is crucial for strengthening vessel walls during angiogenesis and also regulates the proliferation of SMCs, indicating the potential involvement of TGF-β signaling in the pathogenesis and development of cerebral aneurysms. This review examines the complex role of TGF-β, its receptors, and signaling pathways in cerebral aneurysm formation and progression. Understanding the molecular mechanisms of TGF-β signaling in aneurysm development is vital for identifying potential therapeutic targets to prevent aneurysm rupture. Further research is necessary to fully elucidate the role of TGF-β in aneurysm pathophysiology, which could lead to the development of novel therapeutic strategies for aneurysm prevention and management, particularly in preventing subarachnoid hemorrhage.</p> Graphical Abstract <p></p>