A New "Lnc" to Brake Inflammation.

A New "Lnc" to Brake Inflammation.
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抑制炎症的新“Lnc”。

DOI:
10.1161/atvbaha.123.319444
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发表时间:
2023
期刊:
Arteriosclerosis, thrombosis, and vascular biology
影响因子:
--
通讯作者:
Zhou,Jiliang
Zhou,Jiliang
中科院分区:
--
文献类型:
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作者:
Long,Xiaochun;Miano,JosephM;Zhou,Jiliang

文献摘要

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Biological, chemical, and physical perturbations to the vessel wall initiate inflammatory processes intended, initially, to preserve vascular homeostasis. However, if inflammation proceeds unabated or occurs repeatedly in bursts over an extended time period, pathology ensues. For example, unrestrained hyperlipidemia promotes monocyte adhesion to endothelial cells with subsequent diapedesis, differentiation into macrophages licensed to clear infiltrating lipids, and foam cell formation. Chronic vascular inflammation exacerbates these early fatty streaks leading to complicated plaques that may rupture causing catastrophic occlusion of vessels in the heart, brain, and extremities. 1 Endogenous protein encoding anti-inflammatory genes2 and the complicated3 specialized proresolving lipid mediators4 counterbalance vascular inflammation. Elucidating mechanisms of inflammatory resolution to mitigate vascular disease progression has been a major area of focus. Over the past decade, scores of genes that do not encode for proteins have emerged as critical fine tuners of inflammation and inflammatory resolution. 5 Long noncoding RNAs (LncRNAs) are among the more unpredictable class of noncoding genes with functions ranging from the control of splicing, transcription, and structural architecture in the nucleus to translation, signaling, and transport in the cytosol. Although dozens of LncRNAs have roles in stimulating inflammation, comparatively few counteract inflammatory processes. 5–7