Epigenetic Regulation of Autophagy in Bone Metabolism.
autophagy
bone homeostasis
bone metabolism
bone-related diseases
epigenetics
miRNA
Journal
Function (Oxford, England)
ISSN: 2633-8823
Titre abrégé: Function (Oxf)
Pays: England
ID NLM: 101770668
Informations de publication
Date de publication:
2024
2024
Historique:
received:
20
10
2023
revised:
18
01
2024
accepted:
24
01
2024
medline:
18
3
2024
pubmed:
15
3
2024
entrez:
15
3
2024
Statut:
epublish
Résumé
The skeletal system is crucial for supporting bodily functions, protecting vital organs, facilitating hematopoiesis, and storing essential minerals. Skeletal homeostasis, which includes aspects such as bone density, structural integrity, and regenerative processes, is essential for normal skeletal function. Autophagy, an intricate intracellular mechanism for degrading and recycling cellular components, plays a multifaceted role in bone metabolism. It involves sequestering cellular waste, damaged proteins, and organelles within autophagosomes, which are then degraded and recycled. Autophagy's impact on bone health varies depending on factors such as regulation, cell type, environmental cues, and physiological context. Despite being traditionally considered a cytoplasmic process, autophagy is subject to transcriptional and epigenetic regulation within the nucleus. However, the precise influence of epigenetic regulation, including DNA methylation, histone modifications, and non-coding RNA expression, on cellular fate remains incompletely understood. The interplay between autophagy and epigenetic modifications adds complexity to bone cell regulation. This article provides an in-depth exploration of the intricate interplay between these two regulatory paradigms, with a focus on the epigenetic control of autophagy in bone metabolism. Such an understanding enhances our knowledge of bone metabolism-related disorders and offers insights for the development of targeted therapeutic strategies.
Identifiants
pubmed: 38486976
doi: 10.1093/function/zqae004
pii: zqae004
pmc: PMC10935486
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
zqae004Informations de copyright
© The Author(s) 2024. Published by Oxford University Press on behalf of American Physiological Society.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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