Role of MicroRNA-141 in the Aging Musculoskeletal System: A Current Overview
•MIRNA-141 plays a vital role in stem cell senescence.•MIRNA-141 negatively regulated stem cell differentiation.•Oxidative and inflammatory stress factors regulate MiRNA-141.•MiRNA-141 dysregulated with aging and the aging musculoskeletal phenotype.•Antagonists of miR-141 could potentially be therap...
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Veröffentlicht in: | Mechanisms of ageing and development 2019-03, Vol.178, p.9-15 |
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Sprache: | eng |
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Zusammenfassung: | •MIRNA-141 plays a vital role in stem cell senescence.•MIRNA-141 negatively regulated stem cell differentiation.•Oxidative and inflammatory stress factors regulate MiRNA-141.•MiRNA-141 dysregulated with aging and the aging musculoskeletal phenotype.•Antagonists of miR-141 could potentially be therapeutic agents to address age-related musculoskeletal diseases.
MicroRNA’s are small non-coding RNAs that regulate the expression of genes by targeting the 3’ UTR’s of mRNA. Studies reveal that miRNAs play a pivotal role in normal musculoskeletal function such as mesenchymal stem cell differentiation, survivability and apoptosis, osteogenesis, and chondrogenesis. Changes in normal miRNA expression have been linked to a number of pathological disease processes. Additionally, with aging, it is noted that there is dysregulation in the normal function of stem cell differentiation, bone formation/degradation, chondrocyte function, and muscle degeneration. Due to the change in expression of miRNA in degenerative musculoskeletal pathology, it is believed that these molecules may be at least partially responsible for cellular dysfunction. A number of miRNAs have already been identified to play a role in osteoarthritis, osteoporosis and sarcopenia. One miRNA that has become of interest recently is miRNA 141. The purpose of this article is to review the current literature available on miRNA 141 and how it could play a role in osteoporosis, osteoarthritis and musculoskeletal pathology overall. |
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ISSN: | 0047-6374 1872-6216 |
DOI: | 10.1016/j.mad.2018.12.001 |