ArticleExperimental & translational stroke medicine2016
Artery reopening is required for the neurorestorative effects of angiotensin modulation after experimental stroke.
Article in Experimental & translational stroke medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- The role of angiotensin II type 1 receptor pathway in cerebral ischemia‒reperfusion injury: Implications for the neuroprotective effect of ARBs.Neuroprotection (Chichester, England) · 2024Review
- Mechanisms of acute neurovascular protection with AT1 blockade after stroke: Effect of prestroke hypertension.PloS one · 2017Article
- Erratum to: Artery reopening is required for the neurorestorative effects of angiotensin modulation after experimental stroke.Experimental & translational stroke medicine · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
Abstract
backgroundBlood flow restoration with fibrinolysis and thrombectomy is recommended to limit injury in stroke patients with proximal artery occlusion. Angiotensin receptor blockers have been shown to be neuroprotective in models of permanent and temporary occlusion, but the benefits on expression of trophic factors have been seen only when the artery is reopened. It is possible that early artery opening with endovascular intervention may increase the likelihood of identifying an effective combination therapy for patients.
methodsNormotensive male Wistar rats were subjected to mechanical middle cerebral artery occlusion (either temporary or permanent), followed by randomization to receive candesartan (0.3 mg/kg IV) or saline. Functional outcome, infarct size, and biochemical changes were assessed 24 h after ischemia induction.
resultsLack of reperfusion blunted candesartan induced neuroprotection (p < 0.05) and reduced the improvement of functional outcome (p < 0.05). With reperfusion, candesartan increased mature BDNF expression in the contralateral hemisphere (p < 0.05) and activated prosurvival (Akt-GSK3-β) signaling (p < 0.05). Without reperfusion, candesartan significantly reduced VEGF expression and MMP activation and increased NOGO A expression, creating an environment hostile to recovery.
conclusionCandesartan induced pro-recovery effects are dependent on the presence of reperfusion.
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