====== Murine Model of Intracranial Aneurysm ======


{{rss>https://pubmed.ncbi.nlm.nih.gov/rss/search/1RIspYzP7ykSpbKtWeGGUayWk9SbMnm6sTgrf0O876h6pGbIs9/?limit=15&utm_campaign=pubmed-2&fc=20240123071159}}

[[Genetic modification]] in a [[mouse model]] of [[Intracranial Aneurysm]]s, including [[deletion]] or [[overexpression]] of a particular [[gene]], provides an excellent means for examining basic mechanisms behind disease [[pathophysiology]] and developing novel pharmacological approaches. All existing [[animal model]]s need some pharmacological treatments, surgical interventions, or both to develop IAs, which is different from the spontaneous and natural development of aneurysms under the influence of the classical [[risk factor]]s. The benefit of such animal models is the development of IAs in a limited time. However, [[clinical translation]] of the results is often challenging because of the artificial course of IA development and growth. 
Khan et al. summarized the continuous improvement in mouse models of IAs. Moreover, they discussed the pros and cons of existing [[mouse model]]s of IAs and highlighted the main translational roadblocks and how to improve them to increase the success of translational [[Intracranial Aneurysm research]]
((Khan D, Li X, Hashimoto T, Tanikawa R, Niemela M, Lawton M, Muhammad S. Current Mouse Models of [[Intracranial Aneurysm]]s: Analysis of Pharmacological Agents Used to Induce Aneurysms and Their Impact on Translational Research. J Am Heart Assoc. 2024 Jan 23:e031811. doi: 10.1161/JAHA.123.031811. Epub ahead of print. PMID: 38258667.)).
----
[[Intracranial aneurysm rupture]] causes severe disability and high mortality. Epidemiological studies show a strong association between decreased [[vitamin D]] levels and an increase in [[aneurysm rupture]]. However, the [[causality]] and mechanism remain largely unknown. 
Kimura et al. tested whether vitamin D deficiency promotes aneurysm rupture and examined the underlying mechanism for the protective role of vitamin D against the development of aneurysm rupture utilizing a [[mouse model]] of intracranial aneurysm. Mice consuming a vitamin D-deficient [[diet]] had a higher rupture rate than mice with a regular diet. Vitamin D deficiency increased proinflammatory [[cytokine]]s in the cerebral arteries. Concurrently, vitamin D receptor knockout mice had a higher rupture rate than the corresponding wild-type littermates. The vitamin D receptors on endothelial and vascular smooth muscle cells, but not on hematopoietic cells, mediated the effect of aneurysm rupture. The results establish that vitamin D protects against the development of aneurysmal rupture through the vitamin D receptors on vascular endothelial and smooth muscle cells. Vitamin D supplementation may be a viable pharmacologic therapy for preventing aneurysm rupture
((Kimura T, Rahmani R, Miyamoto T, Kamio Y, Kudo D, Sato H, Ikedo T, Baranoski JF, Uchikawa H, Ai J, Lawton MT, Hashimoto T. Vitamin D deficiency promotes intracranial aneurysm rupture. J Cereb Blood Flow Metab. 2024 Jan 19:271678X241226750. doi: 10.1177/0271678X241226750. Epub ahead of print. PMID: 38241458.))