Autophagy: A new player in skeletal maintenance?

Lynne J. Hocking*, Caroline Whitehouse, Miep H. Helfrich

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

141 Citations (Scopus)

Abstract

Imbalances between bone resorption and formation lie at the root of disorders such as osteoporosis, Paget's disease of bone (PDB), and osteopetrosis. Recently, genetic and functional studies have implicated proteins involved in autophagic protein degradation as important mediators of bone cell function in normal physiology and in pathology. Autophagy is the conserved process whereby aggregated proteins, intracellular pathogens, and damaged organelles are degraded and recycled. This process is important both for normal cellular quality control and in response to environmental or internal stressors, particularly in terminally-differentiated cells. Autophagic structures can also act as hubs for the spatial organization of recycling and synthetic process in secretory cells. Alterations to autophagy (reduction, hyperactivation, or impairment) are associated with a number of disorders, including neurodegenerative diseases and cancers, and are now being implicated in maintenance of skeletal homoeostasis. Here, we introduce the topic of autophagy, describe the new findings that are starting to emerge from the bone field, and consider the therapeutic potential of modifying this pathway for the treatment of age-related bone disorders. 

Original languageEnglish
Article numberN/A
Pages (from-to)1439-1447
Number of pages9
JournalJournal of Bone and Mineral Research
Volume27
Issue number7
DOIs
Publication statusPublished - Jul 2012

Keywords

  • AUTOPHAGY
  • BONE
  • OSTEOCLAST
  • OSTEOBLAST
  • OSTEOCYTE
  • VALOSIN-CONTAINING PROTEIN
  • PAGETS-DISEASE
  • UBA DOMAIN
  • OSTEOCLAST FORMATION
  • IN-VIVO
  • UBIQUITIN BINDING
  • MAMMALIAN TARGET
  • BONE-RESORPTION
  • MOUSE MODEL
  • RAPAMYCIN

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