Molecular Actions of Glucocorticoids in Cartilage and Bone During Health, Disease, and Steroid Therapy.
Kerstin HartmannMascha KoenenSebastian SchauerStephanie Wittig-BlaichMubashir AhmadUlrike BaschantJan P TuckermannPublished in: Physiological reviews (2016)
Cartilage and bone are severely affected by glucocorticoids (GCs), steroid hormones that are frequently used to treat inflammatory diseases. Major complications associated with long-term steroid therapy include impairment of cartilaginous bone growth and GC-induced osteoporosis. Particularly in arthritis, GC application can increase joint and bone damage. Contrarily, endogenous GC release supports cartilage and bone integrity. In the last decade, substantial progress in the understanding of the molecular mechanisms of GC action has been gained through genome-wide binding studies of the GC receptor. These genomic approaches have revolutionized our understanding of gene regulation by ligand-induced transcription factors in general. Furthermore, specific inactivation of GC signaling and the GC receptor in bone and cartilage cells of rodent models has enabled the cell-specific effects of GCs in normal tissue homeostasis, inflammatory bone diseases, and GC-induced osteoporosis to be dissected. In this review, we summarize the current view of GC action in cartilage and bone. We further discuss future research directions in the context of new concepts for optimized steroid therapies with less detrimental effects on bone.
Keyphrases
- bone mineral density
- postmenopausal women
- soft tissue
- bone loss
- bone regeneration
- gas chromatography
- genome wide
- oxidative stress
- body composition
- rheumatoid arthritis
- public health
- gene expression
- transcription factor
- extracellular matrix
- diabetic rats
- drug induced
- stem cells
- mass spectrometry
- mental health
- risk factors
- pi k akt
- signaling pathway
- endoplasmic reticulum stress
- liquid chromatography
- replacement therapy
- dna binding
- health promotion