Cellular aging, senescence and autophagy processes in osteoarthritis

Abstract

Osteoarthritis (OA) is the most common form of arthritis and a huge health and financial burden. The prevalence and incidence of OA are likely to rise due to increasing life expectancy. Although the link between aging and OA is well established, little is known about the mechanisms by which aging contributes to OA development. In recent years, progress has been made in understanding the molecular mechanisms of chondrocyte aging and senescence. Aging and senescent chondrocytes display a senescence-associated secretory phenotype (SASP) associated with increased secretion of pro-inflammatory mediators, extracellular matrix degrading enzymes and oxidative stress, all of which can contribute to the development and progression of OA. There is also evidence that autophagy, an essential homeostatic process, declines with aging and during OA. This review will focus on our current understanding of chondrocyte aging, senescence, and autophagy and their potential roles in the development and progression of OA. An understanding of these processes would be very useful in devising strategies to treat OA or to delay its development.