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.
Highlights
Macrophages are a subtype of immune cells that comprise an important fraction of the innate immune system
Other studies in murine bone marrow-derived macrophages demonstrated that the expression of the Long non-coding RNAs (lncRNAs) cardiac and apoptosis-related lncRNA (Carlr) is directly increased by NF-κB activation but, more importantly, its knockdown results in significantly reduced expression levels of several NF-κB-regulated genes, such as the nuclear factor of the kappa light polypeptide gene enhancer in B cells 2, p49/p100 (Nfkb2), prostaglandin-endoperoxide synthase 2 (Ptgs2), interleukin 1 alpha (Il1a), and interleukin 1 beta (Il1b) [127]
Recent studies suggest that lncRNAs play a crucial role in the regulation of myeloid recruitment and lineage determination, as well as innate and adaptive immune functions
Summary
Macrophages are a subtype of immune cells that comprise an important fraction of the innate immune system. A transient hematopoietic wave of erythro-myeloid progenitors (EMPs) emerges from the posterior plate mesoderm and forms yolk sac blood islands These yolk sac-derived macrophages are formed independently of hematopoietic stem/progenitor cells and monocytes. Many signaling pathways have been identified that direct macrophage polarization and function, it is not fully understood how such pathways are regulated; RNA-mediators, such as long non-coding RNAs (lncRNAs), have emerged as important signaling components dictating various aspects of macrophage biology [12,13,14] To this end, here, we review the current knowledge regarding the regulation of macrophage function by lncRNAs in the context of cardiovascular disease (CVD). Compared to other similar review articles in recent years [15,16], we summarize current knowledge regarding lncRNAs in directing various aspects of macrophage functions in CVD, including foam cell formation, Toll-like receptor (TLR) and NF-kβ signaling, and macrophage phenotype switching
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