Epigenetic regulators involved in osteoclast differentiation

Kristina Astleford, Emily Campbell, Andrew Norton, Kim C. Mansky

Research output: Contribution to journalReview articlepeer-review

Abstract

Age related changes to the skeleton, such as osteoporosis, increase the risk of fracture and morbidity in the elderly population. In osteoporosis, bone remodeling becomes unbalanced with an increase in bone resorption and a decrease in bone formation. Osteoclasts are large multinucleated cells that secrete acid and proteases to degrade and resorb bone. Understanding the molecular mechanisms that regulate osteoclast differentiation and activity will provide insight as to how hyper-active osteoclasts lead to pathological bone loss, contributing to diseases such as osteoporosis. Reversible modifications to the DNA such as histone acetylation, methylation, phosphorylation and ubiquitylation alters the access of transcriptional machinery to DNA and regulates gene expression and osteoclast differentiation and activity. It is critical for the management of bone related diseases to understand the role of these chromatin modifying proteins during osteoclast differentiation, as potential therapies targeting these proteins are currently under development.

Original languageEnglish (US)
Article number7080
Pages (from-to)1-15
Number of pages15
JournalInternational journal of molecular sciences
Volume21
Issue number19
DOIs
StatePublished - Oct 1 2020

Bibliographical note

Funding Information:
This research was funded by National Institute of Arthritis and Musculoskeletal and Skin Disease/National Institutes of Health AR061352.

Funding Information:
Funding: This research was funded by National Institute of Arthritis and Musculoskeletal and Skin Disease/National Institutes of Health AR061352.

Publisher Copyright:
© 2020 by the authors. Licensee MDPI, Basel, Switzerland.

Keywords

  • Acetylation
  • Deacetylation
  • Demethylation
  • Epigenetics
  • Methylation
  • Osteoclasts

PubMed: MeSH publication types

  • Journal Article
  • Review

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