Long non-coding RNAs in osteoporosis: from mechanisms of action to therapeutic potential

Abstract Osteoporosis is a clinical disease characterized by decreased bone density due to a disrupted balance between bone formation and resorption, which increases fracture risk and negatively affects the quality of life of a patient. LncRNAs are RNA molecules over 200 nucleotides in length with non-coding potential. Many studies have demonstrated that numerous biological processes involved in bone metabolism are affected. However, the complex mechanisms of action of lncRNAs and their clinical applications in osteoporosis have not yet been fully elucidated. LncRNAs, as epigenetic regulators, are widely involved in the regulation of gene expression during osteogenic and osteoclast differentiation. LncRNAs affect bone homeostasis and osteoporosis development through different signaling pathways and regulatory networks. Additionally, researchers have found that lncRNAs have great potential for clinical application in the treatment of osteoporosis. In this review, we summarize the research results on lncRNAs for clinical prevention, rehabilitation treatment, drug development, and targeted therapy for osteoporosis. Moreover, we summarize the regulatory modes of various signaling pathways through which lncRNAs affect the development of osteoporosis. Overall, these studies suggest that lncRNAs can be used as novel targeted molecular drugs for the clinical treatment of osteoporosis to improve symptoms..

Medienart:

E-Artikel

Erscheinungsjahr:

2023

Erschienen:

2023

Enthalten in:

Zur Gesamtaufnahme - volume:36

Enthalten in:

Human cell - 36(2023), 3 vom: 07. März, Seite 950-962

Sprache:

Englisch

Beteiligte Personen:

Hou, Jianglin [VerfasserIn]
Liu, Da [VerfasserIn]
Zhao, Jihui [VerfasserIn]
Qin, Sen [VerfasserIn]
Chen, Senxiang [VerfasserIn]
Zhou, Zimo [VerfasserIn]

Links:

Volltext [lizenzpflichtig]

Themen:

Bone marrow mesenchymal stromal cells
Long non-coding RNAs
Osteoclasts
Osteogenesis
Osteoporosis

Anmerkungen:

© The Author(s) under exclusive licence to Japan Human Cell Society 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

doi:

10.1007/s13577-023-00888-5

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

SPR050072455