Abstract
Extracellular vesicles (EVs) are complex phospholipidic structures actively released by cells. EVs are recognized as powerful means of intercellular communication since they contain many signaling molecules (including lipids, proteins, and nucleic acids). In parallel, changes in epigenetic processes can lead to changes in gene function and finally lead to disease onset and progression. Recent breakthroughs have revealed the complex roles of non-coding RNAs (microRNAs (miRNAs) and long non-coding RNAs (lncRNAs)) in epigenetic regulation. Moreover, a substantial body of evidence demonstrates that non-coding RNAs can be shuttled among the cells and tissues via EVs, allowing non-coding RNAs to reach distant cells and exert systemic effects. Resident bone cells, including osteoclasts, osteoblasts, osteocytes, and endothelial cells, are tightly regulated by non-coding RNAs, and many of them can be exported from the cells to neighboring ones through EVs, triggering pathological conditions. For these reasons, researchers have also started to exploit EVs as a theranostic tool to address osteoporosis. In this review, we summarize some recent findings regarding the EVs’ involvement in the fine regulation of non-coding RNAs in the context of bone metabolism and osteoporosis.
Highlights
Osteoporosis is defined by the World Health Organization (WHO) as a progressive systemic skeletal disorder with low bone density and deterioration of bone architecture leading to an increased risk of bone fragility and fracture [1,2]
Zhang et al constructed a comprehensive mRNA–Long Non-Coding RNAs (lncRNAs)–miRNA competing endogenous RNA regulatory network to predict the risk of osteoporosis development by analyzing public Gene Expression Omnibus (GEO) microarray profile data [13]
We provide information about the mechanisms and the role of non-coding RNAs in the regulation of gene expression and their link with extracellular vesicles (EVs) in the onset of osteoporosis
Summary
Osteoporosis is defined by the World Health Organization (WHO) as a progressive systemic skeletal disorder with low bone density and deterioration of bone architecture leading to an increased risk of bone fragility and fracture [1,2]. Osteoporosis is not a severe disease per se, the healthcare cost is massive, especially for the management of the fractures resulting from low bone mass, associated with a decreased quality of life and lifespan in aging people. The era of genome-wide association studies (GWAS) clarifies the horizon of the genetic contribution to osteoporosis. Many GWAS have been performed interrogating genetic association with bone mineral density (BMD), implicating more than 90 candidate genes for osteoporosis [9]. In this context, non-coding RNAs were identified as playing a crucial role as a genomic regulatory system in several biological processes of bone metabolism [10,11]. We provide information about the mechanisms and the role of non-coding RNAs in the regulation of gene expression and their link with extracellular vesicles (EVs) in the onset of osteoporosis
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