Autophagy: A new player in skeletal maintenance?

Lynne J Hocking, Caroline Whitehouse, Miep H Helfrich

Research output: Contribution to journalLiterature reviewpeer-review

135 Citations (Scopus)


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. © 2012 American Society for Bone and Mineral Research.
Original languageEnglish
Pages (from-to)1439-1447
Number of pages9
JournalJournal of Bone and Mineral Research
Issue number7
Early online date15 Jun 2012
Publication statusPublished - Jul 2012


  • autophagy
  • bone
  • osteoclast
  • osteoblast
  • osteocyte


Dive into the research topics of 'Autophagy: A new player in skeletal maintenance?'. Together they form a unique fingerprint.

Cite this