Atorvastatin Protects Against Cerebral Aneurysmal Degenerative Pathology by Promoting Endothelial Progenitor Cells (EPC) Mobilization and Attenuating Vascular Deterioration in a Rat Model

Wei, Huijie; Yang, Ming; Yu, Kai; Wang, Dong; Wang, Liang; Wang, Zengguang; Jiang, Rongcai; Zhang, Jianning

doi:10.12659/msm.915005

Cited by 5 publications

(2 citation statements)

References 31 publications

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“…Concurrently elevating the prevalence of endothelial cells and SMCs, as well as downregulating the expression and activity of metalloproteinase-2 and metalloproteinase-9, forestalls damage to and remodeling of the aneurysm wall. Similarly, rosuvastatin can enhance endothelialization at the aneurysm neck in a rat embolization model [96,97], augment the number of endothelial progenitor cells (EPCs), and restrict inflammation of the vascular wall. These findings suggested that statins could confer protection to or facilitate the repair of the aneurysm wall via a multitude of mechanisms, forestalling its expansion and rupture.…”

Section: Lipid Metabolism Disorder As a Therapeutic Target For Iamentioning

confidence: 99%

Intracranial Aneurysms and Lipid Metabolism Disorders: From Molecular Mechanisms to Clinical Implications

Pan,

Shi,

et al. 2023

Biomolecules

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Many vascular diseases are linked to lipid metabolism disorders, which cause lipid accumulation and peroxidation in the vascular wall. These processes lead to degenerative changes in the vessel, such as phenotypic transformation of smooth muscle cells and dysfunction and apoptosis of endothelial cells. In intracranial aneurysms, the coexistence of lipid plaques is often observed, indicating localized lipid metabolism disorders. These disorders may impair the function of the vascular wall or result from it. We summarize the literature on the relationship between lipid metabolism disorders and intracranial aneurysms below.

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Section: Lipid Metabolism Disorder As a Therapeutic Target For Iamentioning

confidence: 99%

Intracranial Aneurysms and Lipid Metabolism Disorders: From Molecular Mechanisms to Clinical Implications

Pan,

Shi,

et al. 2023

Biomolecules

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“…However, the effects of statins on IAs are controversial. Some statins, such as atorvastatin [ 89 ], simvastatin [ 90 ], pitavastatin [ 91 ], and pravastatin [ 92 ] showed protective effects in animal IA models. In contrast, statins have been reported to promote the growth of experimentally-induced IAs in estrogen-deficient rats, although a low dose of pravastatin does reduce the incidence of IA [ 93 ], suggesting a possibility of differential effects by statins, particularly in older female patients with low estrogen levels.…”

Section: Ho-1 In Intracranial Aneurysmmentioning

confidence: 99%

Therapeutic Potential of Heme Oxygenase-1 in Aneurysmal Diseases

et al. 2020

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Abdominal aortic aneurysm (AAA) and intracranial aneurysm (IA) are serious arterial diseases in the aorta and brain, respectively. AAA and IA are associated with old age in males and females, respectively, and if rupture occurs, they carry high morbidity and mortality. Aneurysmal subarachnoid hemorrhage (SAH) due to IA rupture has a high rate of complication and fatality. Despite these severe clinical outcomes, preventing or treating these devastating diseases remains an unmet medical need. Inflammation and oxidative stress are shared pathologies of these vascular diseases. Therefore, therapeutic strategies have focused on reducing inflammation and reactive oxygen species levels. Interestingly, in response to cellular stress, the inducible heme oxygenase-1 (HO-1) is highly upregulated and protects against tissue injury. HO-1 degrades the prooxidant heme and generates molecules with antioxidative and anti-inflammatory properties, resulting in decreased oxidative stress and inflammation. Therefore, increasing HO-1 activity is an attractive option for therapy. Several HO-1 inducers have been identified and tested in animal models for preventing or alleviating AAA, IA, and SAH. However, clinical trials have shown conflicting results. Further research and the development of highly selective HO-1 regulators may be needed to prevent the initiation and progression of AAA, IA, or SAH.

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