Mechanisms underlying glucocorticoid-induced osteocyte dysfunction

Research output: ThesisDoctoral Thesis

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Abstract

The therapeutic functions of Glucocorticoids (GCs) are unfortunately accompanied by severe bone loss. Being the most abundant cell type in bone, osteocytes are highly susceptible to the adverse effects of GC treatment. In this thesis, the deleterious effects of GC on osteocytes and the underlying mechanisms governing these effects were explored and addressed: (1) GC regulates osteocyte-mediated bone modification and exosomal secretion; (2) GC impairs osteocyte communication by inducing autophagy-mediated degradation of Cx43; (3) GC inhibits ER-mediated mitochondrial transfer within the osteocyte processes; and (4) GC induces REDD1 to regulate autophagy via interaction with Akt-mTORC1 signalling.
Original languageEnglish
QualificationDoctor of Philosophy
Awarding Institution
  • The University of Western Australia
Award date25 Sep 2017
DOIs
Publication statusUnpublished - 2017

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