Mitochondrial dysfunction downstream of mechanical overload and ageing has been associated with chondrocyte senescence in osteoarthritis (OA). A study published in Bone Research links mitochondrial dysfunction in osteoarthritic chondrocytes to loss of PDZK1 expression.

Together, these findings prompted Xiaochun Bai, Daozhang Cai and colleagues to investigate the inverse correlation between PDZK1 expression and senescence in chondrocytes. PDZK1-deficient mice had a greater number of senescent chondrocytes and exhibited more-severe OA pathology after destabilization of the medial meniscus by surgery than did their wild-type littermates. Induced expression of PDZK1 rescued the catabolic and senescent phenotype of chondrocytes subjected to mechanical overload and alleviated OA progression in mice.