Osteocytes burn out, give bone a break.

Abstract

The pathogenic mechanisms of chronic kidney disease-induced osteoporosis are not well understood and might involve metabolic alterations and apoptosis of osteocytes. In this issue, Hsu et al. present experimental work in uremic mice and cultured mouse osteoblasts showing that impaired mitochondrial function and mitophagy in osteocytes contribute to chronic kidney disease-associated osteoporosis. They investigate new therapeutic approaches to improve mitochondrial function in the setting of increased uremic toxin levels.