ArticleBiochemistry and biophysics reports2025
DNA hypomethylated modified lncRNA MALAT1 promotes atherosclerotic cardiovascular disease progression through NF-κB signaling pathway regulating cholesterol metabolism and inflammatory response.
Article in Biochemistry and biophysics reports, 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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4 authors.
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Abstract
Atherosclerotic cardiovascular disease (ASCVD) is a major cause of death and disability worldwide. The pathological basis of these conditions is atherosclerosis (AS), which is associated with high mortality and significant morbidity rates. Long non-coding RNAs (lncRNAs) are crucial in various human diseases, including ASCVD; however, the specific mechanisms by which disease-associated lncRNAs are involved in ASCVD are not fully understood. In our study, we observed upregulated expression of metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) and DNA hypomethylation levels in ASCVD patients. To investigate the role of MALAT1 in ASCVD, we used oxidized low-density lipoprotein (ox-LDL)-treated THP-1 macrophages as a cellular model. Functional experiments demonstrated that the knockdown of MALAT1 reversed ox-LDL-mediated inhibition of cell viability, promotion of apoptosis, cholesterol metabolism imbalance, and inflammatory responses. Furthermore, inhibition of MALAT1 ameliorated the progression of AS in ApoE
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