Mechanistic Insight on Autophagy Modulated Molecular Pathways in Cerebral Ischemic Injury: From Preclinical to Clinical Perspective

2022 ◽  
Author(s):  
Palak Kalra ◽  
Heena Khan ◽  
Amarjot Kaur ◽  
Thakur Gurjeet Singh
Keyword(s):  
Ischemic Injury ◽  
Molecular Pathways ◽  
Clinical Perspective ◽  
Mechanistic Insight ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic

Biochemical indices of cerebral ischemic injury

1983 ◽  
Vol 43 (3) ◽  
pp. 261-265 ◽  
Author(s):  
T. Bohmer ◽  
J. Kjekshus ◽  
P. Vaagenes
Keyword(s):  
Ischemic Injury ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic ◽  
Biochemical Indices

scholarly journals Intradialytic Cerebral Hypoperfusion as Mechanism for Cognitive Impairment in Patients on Hemodialysis

2019 ◽  
Vol 30 (11) ◽  
pp. 2052-2058 ◽  
Author(s):  
Dawn F. Wolfgram
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Perfusion ◽  
Ischemic Injury ◽  
Hemodialysis Patients ◽  
Cognitive Outcomes ◽  
Cerebral Injury ◽  
Cerebral Hypoperfusion ◽  
Increased Risk ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic

The high frequency of cognitive impairment in individuals on hemodialysis is well characterized. In-center hemodialysis patients are disproportionately affected by cognitive impairment compared with other dialysis populations, identifying hemodialysis itself as a possible factor. The pathophysiology of cognitive impairment has multiple components, but vascular-mediated cerebral injury appears to contribute based on studies demonstrating increased cerebral ischemic lesions and atrophy in brain imaging of patients on hemodialysis. Patients on hemodialysis may be at increased risk for cerebral ischemic injury disease due to vasculopathy associated with ESKD and from their comorbid diseases, such as hypertension and diabetes. This review focuses on the intradialytic cerebral hypoperfusion that can occur during routine hemodialysis due to the circulatory stress of hemodialysis. This includes a review of current methods used to monitor intradialytic cerebral perfusion and the structural and functional cognitive outcomes that have been associated with changes in intradialytic cerebral perfusion. Monitoring of intradialytic cerebral perfusion may become clinically relevant as nephrologists try to avoid the cognitive complications seen with hemodialysis. Identifying the appropriate methods to assess risk for cerebral ischemic injury and the relationship of intradialytic cerebral hypoperfusion to cognitive outcomes will help inform the decision to use intradialytic cerebral perfusion monitoring in the clinical setting as part of a strategy to prevent cognitive decline.

scholarly journals Artemether confers neuroprotection on cerebral ischemic injury through stimulation of the Erk1/2-P90rsk-CREB signaling pathway

Redox Biology ◽  
2021 ◽  
pp. 102069
Author(s):  
Shuai Li ◽  
Tangming Peng ◽  
Xia Zhao ◽  
Marta Silva ◽  
Linlin Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Ischemic Injury ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic ◽  
Stimulation Of

scholarly journals Curcumin Protects Neuron against Cerebral Ischemia-Induced Inflammation through Improving PPAR-Gamma Function

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Zun-Jing Liu ◽  
Wei Liu ◽  
Lei Liu ◽  
Cheng Xiao ◽  
Yu Wang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Neuronal Damage ◽  
Infarct Volume ◽  
Critical Role ◽  
Ischemic Injury ◽  
Ppar Gamma ◽  
Neurological Deficits ◽  
Protective Effects ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic

Cerebral ischemia is the most common cerebrovascular disease worldwide. Recent studies have demonstrated that curcumin had beneficial effect to attenuate cerebral ischemic injury. However, it is unclear how curcumin protects against cerebral ischemic injury. In the present study, using rat middle cerebral artery occlusion model, we found that curcumin was a potent PPARγagonist in that it upregulated PPARγexpression and PPARγ-PPRE binding activity. Administration of curcumin markedly decreased the infarct volume, improved neurological deficits, and reduced neuronal damage of rats. In addition, curcumin suppressed neuroinflammatory response by decreasing inflammatory mediators, such as IL-1β, TNF-α, PGE2, NO, COX-2, and iNOS induced by cerebral ischemia of rats. Furthermore, curcumin suppressed IκB degradation that was caused by cerebral ischemia. The present data also showed that PPARγinteracted with NF-κB-p65 and thus inhibited NF-κB activation. All the above protective effects of curcumin on cerebral ischemic injury were markedly attenuated by GW9662, an inhibitor of PPARγ. Our results as described above suggested that PPARγinduced by curcumin may play a critical role in protecting against brain injury through suppression of inflammatory response. It also highlights the potential of curcumin as a therapeutic agent against cerebral ischemia.

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