AI Article Synopsis
- Atherosclerosis is a chronic inflammatory disease causing the buildup of fatty lesions in arteries, leading to significant cardiovascular mortality worldwide.
- Recent research suggests that ferroptosis, a type of programmed cell death, may play a role in atherosclerosis, although its mechanisms are not fully understood.
- The study identified 59 ferroptosis-related genes in atherosclerosis, conducted analyses to understand their functions, and constructed networks to explore how these genes interact with non-coding RNAs, helping to uncover potential new therapeutic targets.
Article Abstract
Atheroclerosis refers to a chronic inflammatory disease featured by the accumulation of fibrofatty lesions in the intima of arteries. Cardiovasular events associated with atherosclerosis remain the major causes of mortality worldwide. Recent studies have indicated that ferroptosis, a novel programmed cell death, might participate in the process of atherosclerosis. However, the ferroptosis landscape is still not clear. In this study, 59 genes associated with ferroptosis were ultimately identified in atherosclerosis in the intima. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed for functional annotation. Through the construction of protein-protein interaction (PPI) network, five hub genes (, , , , and ) were then validated histologically. The competing endogenous RNA (ceRNA) network of hub genes was ultimately constructed to explore the regulatory mechanism between lncRNAs, miRNAs, and hub genes. The findings provide more insights into the ferroptosis landscape and, potentially, the therapeutic targets of atherosclerosis.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8766414 | PMC |
| http://dx.doi.org/10.3389/fcell.2021.800833 | DOI Listing |
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