ArticleCommunications biology2025
Modulation of Sel1L can alleviate altered ER homeostasis towards white matter damage in CKD-stroke complex.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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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2 citing papers in PubMed.
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20 authors.
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Abstract
Stroke is one of the major causes of mortality and long-term disability worldwide. Chronic-kidney-disease (CKD) is a condition where patients have shown increased vulnerability to stroke with poor functional and cognitive outcomes. Impaired cerebral autoregulation in CKD patients may impose a high risk of stroke. To date, the mechanism of worsened stroke outcomes in CKD patients are limitedly understood. Alterations of endoplasmic-reticulum (ER) homoeostasis via modification of Sel1L-Hrd1 complex is one of the many cellular events that gets triggered following both CKD and stroke leading to accumulation of misfolded proteins, culminating in ER-stress. Therefore, the present study aims to explore the involvement of Sel1L mediated altered ER functions towards worsening of stroke outcome in CKD and further its crucial role towards white matter damage. CKD-stroke complex was induced in male Sprague-Dawley rats followed by middle-cerebral-artery occlusion. At 24 h and 7
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