2020
DOI: 10.3389/fneur.2020.552470
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Inflammatory Response of Ischemic Tolerance in Circulating Plasma: Preconditioning-Induced by Transient Ischemic Attack (TIA) Phenomena in Acute Ischemia Patients (AIS)

Abstract: Inflammation Response of Prior TIA days before IS. These two proteins showed an earlier inflammation profile that was not detectable by the biomarker panel. Conclusion:Inflammatory pathways were activated by transient ischemic attack, however the period of time between this event and a further ischemic stroke could be determined by a protein signature that would contribute to define the role of ischemic tolerance induced by TIA.

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Cited by 8 publications
(10 citation statements)
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References 62 publications
(69 reference statements)
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“…Recent research revealed that patients whose systolic blood pressure was over 140 mmHg exposed a higher risk of recurring neurological dysfunction (de Havenon et al, 2021). Moreover, studies also discovered that further stroke was more likely to happen in TIA patients with intracranial atherosclerosis and aberrant inflammatory response (Luijendijk et al, 2011;Colas-Campas et al, 2020;Lindenholz et al, 2020). In the previous study, we have proven that overactivated autophagy and apoptosis of neurons could exacerbate cerebral ischemia-reperfusion injury and aggravated neurological impairments (Yu et al, 2020;Yu et al, 2021).…”
Section: Discussionmentioning
confidence: 95%
“…Recent research revealed that patients whose systolic blood pressure was over 140 mmHg exposed a higher risk of recurring neurological dysfunction (de Havenon et al, 2021). Moreover, studies also discovered that further stroke was more likely to happen in TIA patients with intracranial atherosclerosis and aberrant inflammatory response (Luijendijk et al, 2011;Colas-Campas et al, 2020;Lindenholz et al, 2020). In the previous study, we have proven that overactivated autophagy and apoptosis of neurons could exacerbate cerebral ischemia-reperfusion injury and aggravated neurological impairments (Yu et al, 2020;Yu et al, 2021).…”
Section: Discussionmentioning
confidence: 95%
“…On cellular and molecular levels, there are a few mechanisms that might contribute to the IPC in patients with TIAs prior to the stroke events compared with those without TIA history. For example, a few comparative studies demonstrated that patients with TIAs prior to strokes have lower levels of specific inflammatory markers that are known to get elevated as a part of the brain tissue response to ischemia in comparison with patients without TIAs ( 37 , 41 ). Accordingly, it is suggested that TIAs boost the brain capacity to downregulate inflammatory responses, limiting the inflammatory response triggered by ischemic strokes.…”
Section: Discussionmentioning
confidence: 99%
“…Accordingly, it is suggested that TIAs boost the brain capacity to downregulate inflammatory responses, limiting the inflammatory response triggered by ischemic strokes. Consequently, this can lead to better clinical outcomes ( 41 ). Additionally, there are a few other mechanisms of ischemic tolerance that act on cellular and subcellular levels, including new protein synthesis, activation of adenosine A1 receptors leading to the opening of adenosine-triphosphate-dependent potassium channels, stimulation of NMDA receptors, upregulation of antioxidant enzymes, and overexpression of the immediate early genes and apoptosis suppression genes ( 22 , 33 , 50 ).…”
Section: Discussionmentioning
confidence: 99%
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