A systematic review and meta-analysis of risk factors for unruptured intracranial aneurysm growth

Jin, Dianshi; Leng, Xiaolei; Han, Peng

doi:10.1016/j.ijsu.2019.07.023

Cited by 39 publications

(23 citation statements)

References 32 publications

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“…Cerebral aneurysms (CAs) are aberrant structures of the brain vasculature, characterized by a ballooning of blood at a local site, 1 which displays several structural, cellular and molecular changes from the healthy vessel. Constant collagen remodelling is observed in CAs and appears to be accelerated by cigarette smoking and hypertension 2 .…”

Section: Introductionmentioning

confidence: 99%

Circulating Treg cells from patients with cerebral aneurysms displayed deficiency in ICOS expression and function

Zhao

Peng

et al. 2020

Clin Exp Pharma Physio

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Inducible costimulator (ICOS) is a member of the CD28 family. When activated, ICOS signalling promotes FOXP3 CNS2 gene demethylation and stabilizes Treg differentiation. Cerebral aneurysm (CA) is the local ballooning of the cerebral vasculature, characterized by higher levels of inflammation mediators and tissue remodelling. FOXP3+ Treg cell dysfunction may contribute to CA pathogenesis. In this study, the expression and function of ICOS in Treg cells was investigated. Circulating CD4+CD25hi T cells from CA subjects demonstrated significantly lower levels of ICOS expression than circulating CD4+CD25hi T cells from healthy subjects. In both healthy subjects and CA subjects, FOXP3+ Treg cells were highly concentrated in the ICOS+ fraction of CD4+CD25hi T cells. Anti‐ICOS costimulation, in combination with anti‐CD3 and IL‐2, significantly increased FOXP3 expression in CD4+CD25hiICOS+ T cells but not in CD4+CD25hiICOS‐ T cells. In addition, anti‐CD3/IL‐2 and anti‐ICOS costimulation significantly elevated the expression of IL‐10 and TGF‐β, decreased the expression of IL‐17, and enhanced CD4+CD25hiICOS+ T cell‐mediated suppression of autologous CD4+CD25‐ Tconv proliferation. Interestingly, CD4+CD25hiICOS+ T cells from CA subjects presented lower responsiveness toward anti‐ICOS costimulation than CD4+CD25hiICOS+ T cells from healthy subjects. Overall, these results demonstrated that ICOS signalling could significantly improve FOXP3 expression and enhance Treg functional potency. However, circulating Treg cells from CA patients displayed reduced ICOS expression and lower responsiveness toward anti‐ICOS stimulation.

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Section: Introductionmentioning

confidence: 99%

Circulating Treg cells from patients with cerebral aneurysms displayed deficiency in ICOS expression and function

Zhao

Peng

et al. 2020

Clin Exp Pharma Physio

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“…Recent studies have shown that lncRNAs are partially specific for tissue and cell type, suggesting their functional significance. The combination of ECM disruption, dysfunction of ECs, VSMCs phenotypic switching, overproduction of reactive oxygen species (ROS), inflammation, and immune responses, represents a dynamic process that leads to deterioration of the vascular wall and formation of IAs [1]. However, only a few reports cited here were able to provide evidence for a suspected molecular mechanism of action being mediated through lncRNAs.…”

Section: Introductionmentioning

confidence: 86%

“…The characteristic pathology of IAs is characterized by progressive cerebral vessel wall dilation, promoted by dying VSMCs, "aberrant" proliferation, and migration of VSMCs, as well as impaired synthesis and degradation of ECM components, which at least partially is the result of transmural inflammation and its disruptive effect on cerebral vessel wall homeostasis [1]. Currently no conservative treatment approach exists that could slow down IA progression and protect the risk of rupture.…”

Section: Lncrna-based Therapeuticsmentioning

confidence: 99%

“…Intracranial aneurysms (IAs) occur in 2% to 3% of the general population and are characterized by localized structural deterioration of the arterial wall, with loss of the internal elastic lamina and disruption of the media [1]. Rupture of IAs can cause 85% of subarachnoid hemorrhage (SAH), a death of 30-50% of the cases, and a severe disability in 30% of the cases [1,2]. At present, the treatment and prevention of intracranial aneurysms are still challenged due to their unknown pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

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The Role of Long Non-Coding RNAs in Intracranial Aneurysms and Subarachnoid Hemorrhage

Gareev

Beylerli

Aliev

et al. 2020

Life

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Intracranial aneurysms (IAs) represent the most complex and relevant problem of modern neurology and neurosurgery. They serve as one of the main causes of non-traumatic subarachnoid hemorrhage (SAH), causing up to 85% of all cases of intracranial hemorrhage, which is associated with frequent disability and high mortality among patients. Unfortunately, the molecular mechanisms of the development and rupture of IAs are still under study. Long non-coding RNAs (lncRNAs) are non-coding RNAs that typically have a length of more than 200 nucleotides. It is known that lncRNAs regulate many processes, such as transcription, translation, cell differentiation, regulation of gene expression, and regulation of the cell cycle. In recent years, a lot of evidence has established their role in human diseases from oncology to cardiovascular disease. Recent studies have shown that lncRNAs may be involved in the pathogenesis of IAs. The study of lncRNAs and its targets in various pathological conditions of a person is a rapidly developing field, and it is likely that the knowledge obtained from these studies regarding the pathogenesis of intracranial aneurysms will have the potential to use lncRNAs in therapy, as well as in the diagnosis and prediction of high aneurysms risk of rupture.

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“…Intracranial aneurysm (IA), also widely known as brain aneurysm, is a severe cerebrovascular disorder caused by the cerebral vein or artery wall weakness. 1 , 2 IA is commonly treated with ballooning or dilation of local blood vessels. IA may rupture or leak, and the ruptured IA could lead to bleeding in brain tissues, causing hemorrhagic stroke.…”

Section: Introductionmentioning

confidence: 99%

LncRNA SAMMSON Overexpression Suppresses Vascular Smooth Muscle Cell Proliferation via Inhibiting miR-130a Maturation to Participate in Intracranial Aneurysm

Pan

Gao

Wan

et al. 2021

NDT

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Background MiR-130a is a recently identified critical player in vascular smooth muscle cell (VSMC) proliferation, which participates in intracranial aneurysm (IA). However, the involvement of miR-130a in IA and its upstream regulator are unknown. Our preliminary sequencing analysis revealed a close correlation between miR-130a and lncRNA SAMMSON across IA samples. Therefore, we further studied the crosstalk between SAMMSON and miR-130a in IA. Methods SAMMSON and miR-130a expression were measured using RT-qPCR. SAMMSON subcellular location was analyzed with nuclear fractionation assay. Their direct interaction was explored with RNA pull-down assay. The role of SAMMSON in miR-130a maturation was studied with overexpression analysis. VSMC cell proliferation was analyzed with BrdU assay. Results SAMMSON and premature miR-130a were deregulated in IA, while mature miR-130a was upregulated in IA. SAMMSON is localized in both the nucleus and cytoplasm, and direct interaction between SAMMSON and miR-130a was observed. SAMMSON overexpression suppressed miR-130a maturation in VSMCs and reduced the enhancing effects of miR-130a on VSMC cell proliferation. Conclusion SAMMSON is overexpressed in IA and suppresses VSMC proliferation via inhibiting miR-130a maturation.

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A systematic review and meta-analysis of risk factors for unruptured intracranial aneurysm growth

Cited by 39 publications

References 32 publications

Circulating Treg cells from patients with cerebral aneurysms displayed deficiency in ICOS expression and function

Circulating Treg cells from patients with cerebral aneurysms displayed deficiency in ICOS expression and function

The Role of Long Non-Coding RNAs in Intracranial Aneurysms and Subarachnoid Hemorrhage

LncRNA SAMMSON Overexpression Suppresses Vascular Smooth Muscle Cell Proliferation via Inhibiting miR-130a Maturation to Participate in Intracranial Aneurysm

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