AIM2 deletion enhances blood‐brain barrier integrity in experimental ischemic stroke

Xu, Siyi; Bian, Huijie; Shu, Shu; Xia, Shengnan; Gu, Yue; Zhang, Mei-Juan; Xu, Yun; Cao, Xiang

doi:10.1111/cns.13699

Cited by 40 publications

(41 citation statements)

References 41 publications

(95 reference statements)

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“…Furthermore, the exact molecular mechanisms of neuronal ferroptosis caused by accumulated cerebral FA needs to be further studied. Apart from formaldehyde accumulation, other mechanisms such as blood brain barrier damage, 48,49 oxidative stress, 50 excessive mitophagy and neuroinflammation, 51 may also impair neurological function in hypoxia conditions and need to be further explored. Last, only male mice were used in our study.…”

Section: Discussionmentioning

confidence: 99%

Acute high‐altitude hypoxia exposure causes neurological deficits via formaldehyde accumulation

et al. 2022

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Acute high-altitude hypoxia exposure causes multiple adverse neurological consequences, including paralysis, blindness, sleep disturbance, mental disorder, and cognitive impairment. 1 Intellectual abilities such as concentration, perception, executive function, learning, and memory can be impaired, 2 which are caused by neuronal damage due to oxidative stress, inflammation, and other mechanisms. 3 However, the exact cellular and molecular mechanism of neurological dysfunction remains unclear. Therefore, there are no

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Section: Discussionmentioning

confidence: 99%

Acute high‐altitude hypoxia exposure causes neurological deficits via formaldehyde accumulation

et al. 2022

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“…Alternatively, mitochondrion is an organelle that plays roles in energy conversion and metabolism, and its dysfunction is the crucial pathophysiological change in ischemic stroke due to oxygen-glucose deprivation ( 14 ). It was found that a few studies have confirmed that NLRC4 ( 15 ), NLRP1 ( 16 ) and AIM2 ( 17 ) can promote cerebral ischemic injury, but there is no evidence that mitochondria can affect the pathological process of cerebral ischemia through them. Previous studies revealed that mitochondrial dysfunction is a vital event during the NLPR3 inflammasome activation ( 18 - 20 ).…”

Section: Introductionmentioning

confidence: 99%

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

et al. 2022

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Post-ischemic neuroinflammation induced by the innate local immune response is a major pathophysiological feature of cerebral ischemic stroke, which remains the leading cause of mortality and disability worldwide. NLR family pyrin domain containing (NLRP)3 inflammasome crucially mediates post-ischemic inflammatory responses via its priming, activation and interleukin-1β release during hypoxic-ischemic brain damage. Mitochondrial dysfunctions are among the main hallmarks of several brain diseases, including ischemic stroke. In the present review, focus was addressed on the role of mitochondria in cerebral ischemic stroke while keeping NLRP3 inflammasome as a link. Under ischemia and hypoxia, mitochondria are capable of controlling NLRP3 inflammasome-mediated neuroinflammation through mitochondrial released contents, mitochondrial localization and mitochondrial related proteins. Thus, inflammasome and mitochondria may be attractive targets to treat ischemic stroke as well as the several drugs that target the process of mitochondrial function to treat cerebral ischemic stroke. At present, certain drugs have already been studied in clinical trials.

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“…Wang's study showed that MiR‐30a inhibitor restored the loss of occludin in microvessels of ischemic stroke rats and attenuate BBB breakdown and ischemic infarction, which conduced better outcome 26 . Xu's study also showed that ischemic reperfusion injury significantly decreased those of the tight junction (TJ) proteins occludin and ZO‐1, and AIM2 knockdown effectively protected BBB integrity by promoting the expression of occludin and ZO‐1 proteins, 27 and Izawa et al. suggested that inter‐endothelial claudin‐5 expression significantly decreased when β1‐integrin–collagen IV interactions were interrupted and subsequently extended the observations to the loss of ZO‐1 and of occludin at the inter‐endothelial interface, ultimately increasing BBB permeability 28 …”

Section: Discussionmentioning

confidence: 98%

“…Wang's study showed that MiR-30a inhibitor restored the loss of occludin in microvessels of ischemic stroke rats and attenuate BBB breakdown and ischemic infarction, which conduced better outcome. 26 Xu's study also showed that ischemic reperfusion injury significantly decreased those of the tight junction (TJ) proteins occludin and ZO-1, and AIM2 knockdown effectively protected BBB integrity by promoting the expression of occludin and ZO-1 proteins, 27 b Core infarct volume was estimated by CT perfusion imaging. For baseline CT perfusion imaging, thirteen patients were obtained in the END group; 45 were obtained in the non-END group.…”

Section: Discussionmentioning

confidence: 99%

Higher serum occludin after successful reperfusion Is associated with early neurological deterioration

Yuan

Sui

et al. 2022

CNS Neurosci Ther

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Aims Early neurological deterioration (END) is an important factor that affects prognosis in patients with acute ischemic stroke. We explored the relationship between serum occludin levels after successful reperfusion and END in patients treated with endovascular thrombectomy (EVT). Methods We prospectively enrolled 120 stroke patients who underwent EVT with successful reperfusion. Enzyme‐linked immunosorbent assay was used to detect the serum occludin levels on admission and within 1 h after successful reperfusion. Receiver operating characteristic curves (ROC) and regression analysis were used to compare the relationship between serum occludin and END after thrombectomy. Results Among the 120 patients, 36 (30%) experienced END. The END group had higher serum occludin levels than the non‐END group after successful reperfusion [4.31 (3.71–5.38) vs 6.32 (5.88–6.99), p < 0.001]. The ROC curve showed that postoperative serum occludin levels had a significant prediction value for END (AUC: 0.86, p < 0.001). Regression analysis showed that serum occludin was an independent risk factor for END in EVT patients (adjusted odds ratio: 4.46, 95% confidence interval: 1.92–10.32; p < 0.001). Conclusions The higher serum occludin levels were strongly related to END after successful reperfusion. Serum occludin may be an independent risk factor for END in EVT patients.

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AIM2 deletion enhances blood‐brain barrier integrity in experimental ischemic stroke

Abstract: This is an open access article under the terms of the Creat ive Commo ns Attri bution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 40 publications

References 41 publications

Acute high‐altitude hypoxia exposure causes neurological deficits via formaldehyde accumulation

Acute high‐altitude hypoxia exposure causes neurological deficits via formaldehyde accumulation

Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

Higher serum occludin after successful reperfusion Is associated with early neurological deterioration

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