Is mitochondrial oxidative phosphorylation a downstream regulator of nitric oxide effects on chondrocyte matrix synthesis and mineralization?
Chondrocyte mitochondrial reserve, as NO-sensitive mitochondrial respiration-mediated ATP production, appears to support matrix synthesis and PPi elaboration and to regulate MV composition and mineralizing activity. NO-induced depression of chondrocyte respiration could modulate matrix loss and secondary cartilage mineralization in OA.
Our findings indicate that inflammatory activity in the advanced stage of IPF is still relevant, although a Ga(67) scan is not predictive of the clinical course.