Hyperhomocysteinemia as a Risk Factor for Saccular Intracranial Aneurysm: A Cohort Study in a Chinese Han Population

Ren, Jinrui; Ren, Shaohua; Niu, Bo; Wu, Jun; Cao, Yong; Ding, Xiaofeng; Zhen, Zigang; Hao, Xudong; Wang, Shuo

doi:10.1016/j.jstrokecerebrovasdis.2017.01.001

Cited by 18 publications

(15 citation statements)

References 27 publications

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“…As is a destructive disease, the pathogenesis of IA has not been clarified [2]. IA is a rare familial form, but it is generally thought to be the result of acquired vascular injury caused by hypertension, smoking, and other traditional risk factors [3]. Endovascular coiling or microsurgical clipping have been utilized to prevent future rupture of unruptured aneurysm in patients with high risk of rupture [4].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Restored microRNA-133a-3p or Depleted PSAT1 Restrains Endothelial Cell Damage-Induced Intracranial Aneurysm Via Suppressing the GSK3β/β-Catenin Pathway

et al. 2020

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It is unclear about the functional role of microRNA-133a-3p (miR-133a-3p) in intracranial aneurysm (IA). Hence, the aim of the present study was to investigate the regulatory role of miR-133a-3p on the regulation of vascular endothelial injury-induced IA through phosphoserine aminotransferase 1 (PSAT1)/glycogen synthase kinase 3β (GSK3β)/β-catenin signaling pathway. Normal intracranial arteriole tissues and IA tissues were gathered from patients with brain trauma and IA. The expression of miR-133a-3p, PSAT1, GSK3β, and β-catenin in tissues was determined by RT-qPCR and western blot analysis. The endothelial cells (ECs) of the human IA were cultured and treated with miR-133a-3p mimic and si-PSAT1 to determine their functions in endothelial cell migration, apoptosis, and proliferation. The expression of miR-133a-3p, PSAT1, GSK3β, β-catenin, Ki-67, CyclinD1, Bax, and Bcl-2 in ECs were tested by RT-qPCR or western blot analysis. Moreover, IA rat model was established to detect the pathological changes and the expression of miR-133a-3p, PSAT1, GSK3β, β-catenin, VEGF, and MMP-9 in IA tissues in vivo. Expression of miR-133a-3p was related to the number and size of IA. MiR-133a-3p expression was deceased and the PSAT1, GSK3β, and β-catenin expression was raised in IA. Restored miR-133a-3p and depleted PSAT1 alleviated the pathological change; reduced PSAT1, GSK3β, and β-catenin expression in IA; suppressed apoptosis and advanced proliferation and migration of IA ECs, as well as reduced VEGF and MMP-9 expression in IA tissues in vivo. Our study suggests that overexpression of miR-133a-3p or downregulation of PSAT1 restrains endothelial cell damage and advances endothelial cell proliferation via inhibiting the GSK3β/β-catenin pathway in IA. MiR-133a-3p might be a potential candidate marker and therapeutic target for IA.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Restored microRNA-133a-3p or Depleted PSAT1 Restrains Endothelial Cell Damage-Induced Intracranial Aneurysm Via Suppressing the GSK3β/β-Catenin Pathway

et al. 2020

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“…47,48 Vitamin B12 deficiency leads to increased homocysteine concentration and can cause vascular damage. 49,50 Given the importance of the stomach in metabolic and micronutrient hemostasis, such changes might affect other systems outside the stomach, such as the circulatory system, and the occurrence of stroke. Our study confirmed previously documented stroke risk factors 6,7 in a cohort of patients with gastrointestinal symptoms, including positive associations of stroke with increased age, male sex, hypertension, and AF.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori infection and prevalence of stroke

et al. 2018

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Background Helicobacter pylori causes peptic ulcer disease; however, conflicting evidence exists regarding its role in extragastric conditions. We aimed to examine associations of H pylori infection and peptic ulcer disease with stroke. Methods A cross‐sectional study was undertaken using data of 147 936 individuals aged 25‐95 years who underwent the urea breath test during 2002‐2012, based on the computerized database of the second largest health maintenance organization in Israel. Logistic regression models were fitted to control for potential confounders. Results Overall, 1397 (0.9%) patients had stroke and 76 965 (52.0%) had a H pylori positive test. The likelihood of prevalent stroke increased in relation to H pylori infection: adjusted odds ratio (aOR) 1.16 (95% confidence intervals [CI]: 1.04‐1.29), gastric ulcer: aOR 1.50 (95% CI: 1.18‐1.91), and duodenal ulcer: aOR 1.25 (95% CI: 1.07‐1.46). Conclusions The results support the premise that stroke may be associated with a history of H pylori infection.

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“…The serum homocysteine level was significantly higher in group of patients with intracranial aneurysms compared to aneurysm-free controls (19.98 ± 10.84 µmol/L vs. 15.13 ± 5.55 µmol/L; p<0.001). Total Hcy level >15 µmol/L was associated with higher risk of CA development (adjusted OR 2.196; 95% CI 1.188-4.057; p=0.012) [36]. Nevertheless, in a study performed by Rosi et al [37] in Brazil, median homocysteine serum level was similar in group of patients with CA in comparison with controls ( Elevated Hcy levels may result from nutritional deficiencies of folate, vitamin B 6 and B 12 .…”

Section: Nomentioning

confidence: 96%

“…Although the results of studies concerning the beneficial effects of reduction of serum Hcy on cardiovascular diseases and mortality are not conclusive, it appears that adequate vitamin B intake may possibly protect from intracranial aneurysm formation. Ren et al [36] observed that serum homocysteine level was negatively correlated with vitamin B 12 and folate levels in group of individuals with CAs (r=-0.531; p<0.001 and r=-0.349; p<0.001, respectively). In a study performed by Korai et al [22] folic acid eliminated the unfavorable effect of methionine on aneurysm growth in rats, what indicates a relationship between elevate Hcy level and CAs formation.…”

Section: Nomentioning

confidence: 99%

Role of diet-related factors in cerebral aneurysm formation and rupture

Czekajło

2019

Rocz Panstw Zakl Hig

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Cerebral aneurysms (CAs) are dilations of the wall of an artery in the brain filled with blood. The prevalence of unrupted CA in general population is estimated at approximately 3%. Ruptured aneurysms are the cause of 85% of spontaneous subarachnoid hemorrhage (SAH) cases. The formation of cerebral aneurysms results from various factors, including chronic inflammation, hemodynamic stress and vascular wall remodeling. Reactive oxygen species may induce the endothelial dysfunction possibly through the activation of Nuclear Factor Kappa-B, which is a key regulator of the proinflammatory genes. Hypertension may additionally increase the hemodynamic stress and activate the local renin-angiotensin system. The aim of this review was to assess the role of selected diet-related factors in the formation and rupture of cerebral aneurysms. It appears that inadequate intake of dietary antioxidants, hyperhomocysteinemia, hypertension (including incidental elevated blood pressure) and alcohol consumption may increase the risk of intracranial aneurysms. Individuals at high risk of CA formation and/or rupture should consume adequate amounts of antioxidant vitamins (vitamin C, vitamin E and carotenoids), B vitamins (vitamin B 6 , vitamin B 12 and folate), flavonoids and n-3 fatty acids, limit alcohol and caffeine consumption and regularly control their blood pressure. Vegetables, fruits, grains, pulses, nuts and fish, as well as herbs, spices and tea, should be the major components of the daily diet. Due to the synergistic effect of various dietary components on health, Mediterranean diet or Dietary Approach to Stop Hypertension (DASH) diet, as they meet abovementioned requirements and have high anti-inflammatory potential, are thus recommended for the prevention of cerebral aneurysm formation and rupture. STRESZCZENIETętniaki mózgu to ograniczone poszerzenia światła naczynia krwionośnego wypełnione krwią. Występowanie tętniaków mózgu w ogólnej populacji wynosi około 3%, a pęknięcie tętniaka jest przyczyną 85% przypadków krwotoku do przestrzeni podpajęczynówkowej. Na powstanie tętniaka mózgu wpływa wiele czynników, w tym przewlekły stan zapalny, stres hemodynamiczny i przebudowa ścian naczyń mózgowych. Reaktywne formy tlenu mogą nasilać dysfunkcję śródbłonka m.in. poprzez aktywację jądrowego czynnika transkrypcyjnego NF-κB, który jest głównym regulatorem genów związanych z przebiegiem procesu zapalnego. Ponadto wysokie ciśnienie tętnicze krwi może nasilać stres hemodynamiczny oraz aktywować lokalny układ renina-angiotensyna-aldosteron. Celem artykułu był przegląd piśmiennictwa dotyczącego roli wybranych czynników związanych z dietą i z ryzykiem powstania i pęknięcia tętniaków mózgu. Wydaje się, że niewystarczająca podaż składników o działaniu antyoksydacyjnym, hiperhomocysteinemia, nadciśnienie tętnicze (w tym nagłe skoki ciśnienia tętniczego krwi) oraz spożycie alkoholu mogą zwiększać ryzyko rozwoju tętniaków mózgu. Osoby o podwyższonym ryzyku powstania i/lub pęknięcia tętniaka mózgu powinny więc stosować dietę o odpowiedniej zaw...

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Hyperhomocysteinemia as a Risk Factor for Saccular Intracranial Aneurysm: A Cohort Study in a Chinese Han Population

Cited by 18 publications

References 27 publications

RETRACTED ARTICLE: Restored microRNA-133a-3p or Depleted PSAT1 Restrains Endothelial Cell Damage-Induced Intracranial Aneurysm Via Suppressing the GSK3β/β-Catenin Pathway

RETRACTED ARTICLE: Restored microRNA-133a-3p or Depleted PSAT1 Restrains Endothelial Cell Damage-Induced Intracranial Aneurysm Via Suppressing the GSK3β/β-Catenin Pathway

Helicobacter pylori infection and prevalence of stroke

Role of diet-related factors in cerebral aneurysm formation and rupture

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