ArticleRenal failure2025
Defective autophagy in vascular smooth muscle cells promote uremic accelerated atherosclerosis.
Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Beclin 1 level combined with Gensini score and low-density lipoprotein cholesterol correlate strongly with multi-vessel disease.American journal of translational research · 2026Article
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5 authors.
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Abstract
Individuals with chronic kidney disease (CKD) exhibit a significantly elevated risk of premature mortality, predominantly attributable to cardiovascular etiologies. Atherosclerosis is a multifactorial vascular pathology driven by dysregulated lipid metabolism. Notably, patients with CKD exhibit an accelerated progression of atherosclerosis, a condition referred to as uremia-accelerated atherosclerosis (UAAS). Autophagy represents an evolutionarily conserved cellular process that plays a pivotal role in maintaining intracellular homeostasis across cardiovascular cell types. However, the involvement of autophagy in UAAS remains unclear. This study aimed to determine the underlying mechanisms of autophagy in the regulation of UAAS. Autophagy-related differentially expressed genes in UAAS were identified by bioinformatic analysis of GSE135626 dataset. Enrichment analysis showed that autophagy-related DEGs were significantly enriched in regulation of autophagy and PI3K/PKB pathway. Western blotting was used to detect the protein expression levels of Beclin 1, P62, and LCII, and phosphorylation of PI3K and PKB. The result showed that the autophagy level and the phosphorylation levels of PI3K and PKB were decreased in the UAAS group.
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