Abstract
MicroRNAs (miRNAs) are a class of endogenous, non-coding, single-stranded RNAs with a length of approximately 22 nucleotides that are found in eukaryotes. miRNAs are involved in the regulation of cell differentiation, proliferation, invasion, apoptosis, and metabolism by regulating the expression of their target genes. Emerging studies have suggested that various miRNAs play key roles in the pathogenesis of central nervous system (CNS) disorders and may be viable therapeutic targets. In particular, miR-21 has prominently emerged as a focus of increasing research on the mechanisms of its involvement in CNS disorders. Herein, we reviewed recent studies on the critical roles of miR-21, including its dysregulated expression and target genes, in the regulation of pathophysiological processes of CNS disorders, with a special focus on apoptosis and inflammation. Collectively, miR-21 is a versatile regulator in the progression of CNS disorders and could be a promising biomarker and therapeutic target for these diseases. An in-depth understanding of the mechanisms by which miR-21 affects the pathogenesis of CNS disorders could pave the way for miR-21 to serve as a therapeutic target for these conditions.
Highlights
Central nervous system (CNS) disorders are important causes of disability and death worldwide (De Feo et al, 2012)
We focused on the roles of miR-21 in central nervous system (CNS) disorders and its regulatory mechanisms in pathophysiological processes, especially in the context of apoptosis and neuroinflammatory responses
Our review illustrates the important potential of miR-21 as a diagnostic biomarker and therapeutic target in CNS disorders
Summary
Central nervous system (CNS) disorders are important causes of disability and death worldwide (De Feo et al, 2012). Upregulated miR-21 alleviated the cognitive deficits and pathological changes in APP/PS1 mice, suggesting that the intervention in inflammatory responses by regulating miR-21 expression may be a new approach for the treatment of AD (Cui et al, 2018).
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