Back to Search Start Over

The miR‐181 family: Wide‐ranging pathophysiological effects on cell fate and function

Authors :
Austin Bell‐Hensley
Samarjit Das
Audrey McAlinden
Source :
J Cell Physiol
Publication Year :
2023
Publisher :
Wiley, 2023.

Abstract

MicroRNAs (miRNAs) are epigenetic regulators that can target and inhibit translation of multiple mRNAs within a given cell type. As such, a number of different pathways and networks may be modulated as a result. In fact, miRNAs are known to regulate many cellular processes including differentiation, proliferation, inflammation and metabolism. This review focuses on the miR-181 family and provides information from the published literature on the role of miR-181 homologs in regulating a range of activities in different cell types and tissues. Of note, we have not included details on miR-181 expression and function in the context of cancer since this is a broad topic area requiring independent review. Instead, we have focused on describing the function and mechanism of miR-181 family members on differentiation toward a number of cell lineages in various non-neoplastic conditions (e.g. immune/hematopoietic cells, osteoblasts, osteoclasts, chondrocytes, adipocytes). We have also provided information on how modulation of miR-181 homologs can have positive effects on disease states such as cardiac abnormalities, pulmonary arterial hypertension, thrombosis, osteoarthritis and vascular inflammation. In this context, we have used some examples of FDA-approved drugs that modulate miR-181 expression. We conclude by discussing some common mechanisms by which miR-181 homologs appear to regulate a number of different cellular processes and how targeting specific miR-181 family members may lead to attractive therapeutic approaches to treat a number of human disease or repair conditions, including those associated with the aging process.

Details

ISSN :
10974652 and 00219541
Volume :
238
Database :
OpenAIRE
Journal :
Journal of Cellular Physiology
Accession number :
edsair.doi.dedup.....12ba816d5a5e00de81ac538ce424a8f4
Full Text :
https://doi.org/10.1002/jcp.30969