The Regulatory Functions of lncRNAs on Angiogenesis Following Ischemic Stroke

Abstract

Ischemic stroke is one of the leading causes of global mortality and disability. It is a multi-factorial disease involving multiple factors, and gene dysregulation is considered as the major molecular mechanisms underlying disease progression. Angiogenesis can promote collateral circulation, which helps the restoration of blood supply in the ischemic area and reduces ischemic necrosis following ischemic injury. Aberrant expression of long non-coding RNAs (lncRNAs) in ischemic stroke is associated with various biological functions of endothelial cells and serves essential roles on the angiogenesis of ischemic stroke. The key roles of lncRNAs on angiogenesis suggest their potential as novel therapeutic targets for future diagnosis and treatment. This review elucidates the detailed regulatory functions of lncRNAs on angiogenesis following ischemic stroke through numerous mechanisms, such as interaction with target microRNAs, downstream signaling pathways and target molecules.

Keywords: angiogenesis; endothelial cells; ischemic stroke; long non-coding RNAs; therapeutic targets.

Figure 1

The regulatory mechanisms of lncRNAs in ischemic stroke-induced angiogenesis. Some lncRNAs serve essential roles on angiogenesis after ischemic stroke by regulating inflammation, autophagy and apoptosis of BMECs, or directly regulating angiogenesis-associated proteins/signaling pathways to maintain vascular function and integrity. Certain lncRNA may regulate the expression of multiple target genes in various pathways involved in angiogenesis.