Comprehensive analysis of autophagy-related gene expression profiles identified five gene biomarkers associated with immune infiltration and advanced plaques in carotid atherosclerosis

Ma, Ce; Lu, Taoyuan; He, Yanyan; Guo, Dehua; Duan, Lin; Jia, Rufeng; Cai, Dongyang; Gao, Tao; Chen, Zhongcan; Xue, Binghua; Li, Tianxiao; He, Yingkun

doi:10.1186/s13023-023-02660-2

Cited by 6 publications

(5 citation statements)

References 43 publications

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“…Benchmark laboratory data from other groups are in line with the aforementioned findings [30,33]. Notably, MYD88 deficiency has been shown to result in formation of smaller atherosclerotic plaques.…”

Section: Discussionsupporting

confidence: 81%

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Myocardial Expression of Pluripotency, Longevity, and Proinflammatory Genes in the Context of Hypercholesterolemia and Statin Treatment

Mylonas,

Peroulis,

Kapetanakis

et al. 2024

JCM

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Background: This study sought to assess the effect of statin therapy on myocardial inflammation in a White New Zealand rabbit model of atherogenesis. Methods: The mRNA expression levels of pro-inflammatory, pluripotency, and aging-related markers were quantified following a controlled feeding protocol and statin treatments. Results: Following high-cholesterol diet induction, we observed significant upregulation in the myocardial mRNA levels of MYD88, NF-κB, chemokines (CCL4, CCL20, and CCR2), IFN-γ, interleukins (IL-1β, IL-2, IL-4, IL-8, IL-10, and IL-18), and novel markers (klotho, KFL4, NANOG, and HIF1α). In contrast, HOXA5 expression was diminished following a hyperlipidemic diet. Both statin treatments significantly influenced the markers studied. Nevertheless, rosuvastatin administration resulted in a greater reduction in MYD88, NF-kB, chemokines (CCL4, CCL20, and CCR2), and interleukins IL-1β, IL-8, KLF4, NANOG, and HIF1α than fluvastatin. Fluvastatin, on the other hand, led to a stronger decrease in IL-4. Downregulation of IL-2 and IL-18 and upregulation of IFNβ and HOXA5 were comparable between the two statins. Notably, rosuvastatin had a stronger effect on the upregulation of klotho and IL-10. Conclusion: Overall, statin therapy significantly attenuated inflammatory, pluripotency, and klotho expression in myocardial tissue under atherogenic conditions. Our findings also highlight the differential efficacy of rosuvastatin over fluvastatin in curtailing proatherogenic inflammation, which could have profound implications for the clinical management of cardiovascular disease.

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Section: Discussionsupporting

confidence: 81%

“…Chemokines CCL4, CCL20, and CCR2 are implicated in leukocyte recruitment and endothelial interaction [10,[28][29][30]. Their myocardial mRNA levels peaked at G120, corresponding with the heightened inflammatory and immune cell recruitment activity associated with advanced atherogenic stages.…”

Section: Discussionmentioning

confidence: 99%

Myocardial Expression of Pluripotency, Longevity, and Proinflammatory Genes in the Context of Hypercholesterolemia and Statin Treatment

Mylonas,

Peroulis,

Kapetanakis

et al. 2024

JCM

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“…In this study, the carotid AS dataset GSE43292 and GSE125771 configuration files were downloaded from the gene expression omnibus database ( http://www.ncbi.nlm.nih.gov/geo/ ) generated by GPL6244 and GPL17586. GSE43292 includes 32 carotid AS and 32 normal samples, and GSE125771 includes 40 carotid AS samples [ 13 ] to identify differentially expressed genes (DEGs) of carotid AS.…”

Section: Methodsmentioning

confidence: 99%

Higher expression of PLEK and LY86 as the potential biomarker of carotid atherosclerosis

Zhao,

Liu,

et al. 2023

Medicine

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Carotid atherosclerosis (AS) occurs in atherosclerotic lesions of the carotid artery, which can lead to transient ischemic attack and stroke in severe cases. However, the relationship between pleckstrin (PLEK) and lymphocyte antigen 86 (LY86) and carotid AS remains unclear. The carotid AS datasets GSE43292 and GSE125771 were downloaded from the gene expression omnibus database. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis was performed. Construction and analysis of protein-protein interaction network. Functional enrichment analysis, gene set enrichment analysis and comparative toxicogenomics database analysis were performed. TargetScan screened miRNAs that regulated central DEGs. A total of 305 DEGs were identified. According to gene ontology analysis, they were mainly enriched in immune system processes, extracellular regions and cytokine binding. Kyoto encyclopedia of genes and genomes analysis showed that the target cells were mainly enriched in Rap1 signal pathway, B cell receptor signal pathway and PPAR signal pathway. In the enrichment project of metascape, the reaction to bacteria, cell activation and chemotaxis can be seen in the enrichment project of gene ontology. Total 10 core genes (TYROBP, FCER1G, PLEK, LY86, IL10RA, ITGB2, LCP2, FCGR2B, CD86, CCR1) were obtained by protein-protein interaction network construction and analysis. Core genes (PLEK, LY86, IL10RA, ITGB2, and LCP2) were highly expressed in carotid AS samples and lowly expressed in normal samples. Comparative toxicogenomics database analysis showed that 5 genes were associated with pneumonia, inflammation, necrosis, and drug allergy. PLEK and LY86 genes are highly expressed in carotid AS. The higher the expression of PLEK and LY86, the worse the prognosis is.

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“…Figure 6 provides a protein network-centered view of Table 4 and shows that proteins regulating vitamin D's non-genomic pharmacology can physically interact and affect atherosclerosis by regulating the balance between autophagy ( 121 ), apoptosis ( 122 ), endoplasmic reticulum stress response ( 94 ), cellular senescence ( 123 , 124 ), and tissue homeostasis ( 125 ).…”

Section: Resultsmentioning

confidence: 99%

Effects of vitamin D signaling in cardiovascular disease: centrality of macrophage polarization

Fliri,

Kajiji

2024

Front. Cardiovasc. Med.

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Among the leading causes of natural death are cardiovascular diseases, cancer, and respiratory diseases. Factors causing illness include genetic predisposition, aging, stress, chronic inflammation, environmental factors, declining autophagy, and endocrine abnormalities including insufficient vitamin D levels. Inconclusive clinical outcomes of vitamin D supplements in cardiovascular diseases demonstrate the need to identify cause-effect relationships without bias. We employed a spectral clustering methodology capable of analyzing large diverse datasets for examining the role of vitamin D's genomic and non-genomic signaling in disease in this study. The results of this investigation showed the following: (1) vitamin D regulates multiple reciprocal feedback loops including p53, macrophage autophagy, nitric oxide, and redox-signaling; (2) these regulatory schemes are involved in over 2,000 diseases. Furthermore, the balance between genomic and non-genomic signaling by vitamin D affects autophagy regulation of macrophage polarization in tissue homeostasis. These findings provide a deeper understanding of how interactions between genomic and non-genomic signaling affect vitamin D pharmacology and offer opportunities for increasing the efficacy of vitamin D-centered treatment of cardiovascular disease and healthy lifespans.

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Comprehensive analysis of autophagy-related gene expression profiles identified five gene biomarkers associated with immune infiltration and advanced plaques in carotid atherosclerosis

Cited by 6 publications

References 43 publications

Myocardial Expression of Pluripotency, Longevity, and Proinflammatory Genes in the Context of Hypercholesterolemia and Statin Treatment

Myocardial Expression of Pluripotency, Longevity, and Proinflammatory Genes in the Context of Hypercholesterolemia and Statin Treatment

Higher expression of PLEK and LY86 as the potential biomarker of carotid atherosclerosis

Effects of vitamin D signaling in cardiovascular disease: centrality of macrophage polarization

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