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Review
. 2020 Jul 11;6(3):28.
doi: 10.3390/ncrna6030028.

Macrophage Long Non-Coding RNAs in Pathogenesis of Cardiovascular Disease

Affiliations
Review

Macrophage Long Non-Coding RNAs in Pathogenesis of Cardiovascular Disease

Marcin Wysoczynski et al. Noncoding RNA. .

Abstract

Chronic inflammation is inextricably linked to cardiovascular disease (CVD). Macrophages themselves play important roles in atherosclerosis, as well as acute and chronic heart failure. Although the role of macrophages in CVD pathophysiology is well-recognized, little is known regarding the precise mechanisms influencing their function in these contexts. Long non-coding RNAs (lncRNAs) have emerged as significant regulators of macrophage function; as such, there is rising interest in understanding how these nucleic acids influence macrophage signaling, cell fate decisions, and activity in health and disease. In this review, we summarize current knowledge regarding lncRNAs in directing various aspects of macrophage function in CVD. These include foam cell formation, Toll-like receptor (TLR) and NF-kβ signaling, and macrophage phenotype switching. This review will provide a comprehensive understanding concerning previous, ongoing, and future studies of lncRNAs in macrophage functions and their importance in CVD.

Keywords: cardiovascular disease; inflammation; lncRNA; macrophage.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Long non-coding RNAs (LncRNAs) regulate macrophage-derived foam cell formations. LncRNAs (blue) have positive (+) and negative (-) impacts on the expressions of scavenger receptor CD36 and reverse cholesterol transporters ABCA1 and ABCG1 in macrophages (details in text). Ox-LDL: oxidized low-density lipoproteins, HDL: high-density lipoproteins, FC: free cholesterol, LAL: lysosomal acid lipase, and CE: cholesteryl esters.
Figure 2
Figure 2
The impact of lncRNAs on Toll-like receptor (TLR) expressions and nuclear factor (NF)-κB signaling in macrophages. LncRNAs (blue) enhance (+) NF-κB signaling and proinflammatory gene expressions in macrophages (details in text).

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