AGE-induced BMSC apoptosis

Diabetic humans and animals exhibit lower bone mass and healing, resulting from diminished bone formation. Weinberg and colleagues recently reported that type 1 diabetic rats have fewer bone marrow osteoprogenitor cells, and since the formation of advanced glycation end products (AGEs) in bone increases in diabetes, they explored possible mechanisms involved in AGE-induced apoptosis of rat bone marrow stromal cells (BMSCs). They found that AGE increases the apoptosis of BMSCs via the activation of caspases, TNFα production/secretion, p38 MAPK signaling, and oxidative stress. These mechanisms may significantly contribute to the development of osteopenia in diabetic animals.

Read the full article at Weinberg et al. (2014) Journal of Molecular Endocrinology 51; 67–76; DOI:10.1530/JME-13-0229