ArticleArchives of medical science : AMS2024
Abnormal TPM2 expression is involved in regulation of atherosclerosis progression via mediating RhoA signaling
Article in Archives of medical science : AMS, 2024. 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.
- Novel examples of NMD escape through alternative intronic polyadenylation.NAR genomics and bioinformatics · 2026Article
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Authors and funding
6 authors.
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Abstract
Introduction: Ox-LDL (oxidized low-density lipoprotein)-induced endothelial cell injury and dysfunction of vascular smooth muscle cells play critical roles in the development of atherosclerosis (AS). Tropomyosin 2 (TPM2) has been implicated in cardiac diseases, but its critical role and regulatory mechanism in AS progression have not yet been elucidated. Material and methods: The expression of TPM2 was investigated in AS tissues. Ox-LDL was used to construct an AS Results: Tropomyosin 2 was dramatically upregulated in both AS tissues and ox-LDL-induced HAECs. Overexpression of TPM2 attenuated ox-LDL-stimulated cell growth depression, inflammatory and adhesive responses in HAECs, as well as oxidative stress and mitochondrial dysfunction. Additionally, VSMCs, impacted by TPM2-overexpressed HAECs, showed alleviated cellular processes which were abnormally activated by ox-LDL. Furthermore, depressed activation of the RhoA pathway was found in TPM2-overexpressed HAECs and activating the signaling rescued these effects of TPM2 exerted on ox-LDL-stimulated HAECs and VSMCs. Conclusions: TPM2 had an advantageous impact on ox-LDL-induced AS progression
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