New Developments in Exosomal lncRNAs in Cardiovascular Diseases.

Zhu Yuan,Weiqiang Huang

doi:10.3389/fcvm.2021.709169

Abstract

Long non-coding RNAs (lncRNAs) are non-coding RNAs with lengths >200 nt and are involved in the occurrence and development of cardiovascular diseases (CVDs). Exosomes are secreted and produced by various cell types. Exosome contents include various ncRNAs, proteins and lipids. Exosomes are also important mediators of intercellular communication. The proportion of lncRNAs in exosomes is low, but increasing evidence suggests that exosomal lncRNAs play important roles in CVDs. We focused on research progress in exosomal lncRNAs in atherosclerosis, myocardial infarction, myocardial ischemia-reperfusion injury, cardiac angiogenesis, cardiac aging, rheumatic heart disease, and chronic kidney disease combined with CVD. The potential diagnostic and therapeutic effects of exosomal lncRNAs in CVDs are summarized based on preclinical studies involving animal and cell models and circulating exosomes in clinical patients. Finally, the challenges and possible prospects of exosomes and exosomal lncRNAs in clinical applications related to CVD are discussed.

Highlights

Cardiovascular disease (CVD) is currently one of the main causes of death worldwide [1], and atherosclerosis and coronary heart disease are still representative challenges in CVD
This review focuses on the relationship between exosomal lncRNAs and CVD, including the production of exosomal lncRNAs and their mechanism in CVD
Che et al found that the exosomal lncRNA NEAT1 secreted by migration inhibitory factor (MIF)-induced human adipose mesenchymal stem cells (ADMSCs) inhibits H2O2-induced cardiomyocyte apoptosis

Summary

Introduction

Cardiovascular disease (CVD) is currently one of the main causes of death worldwide [1], and atherosclerosis and coronary heart disease are still representative challenges in CVD. Che et al found that the exosomal lncRNA NEAT1 secreted by migration inhibitory factor (MIF)-induced human adipose mesenchymal stem cells (ADMSCs) inhibits H2O2-induced cardiomyocyte apoptosis. Sun et al performed cell and animal experiments and showed that the exosomal lncRNA UCA1 secreted by hypoxia-induced human bone marrow MSCs (BMSCs) sponges MIR-873-5p, regulates XIAP, and enhances AMPK phosphorylation in cardiomyocytes.

Results

Conclusion