Disruption of epoxide hydrolysis inducing oxidative stress and cellular senescence is a novel mechanism responsible for lipoatrophic monogenic diabetes.

Disruption of the intracellular vimentin network upon cellular stress results in enhanced cell surface vimentin on human osteoarthritic chondrocytes and might represent a novel membrane-associated marker of stress-induced premature senescence.

Aging is associated with stress-induced senescence of adipose stromal cells, leading to impaired adipogenesis, oxidative stress, mitochondrial dysfunction, and insulin resistance, all being alleviated by metformin treatment of adipose stromal cells.

The Rho kinases ROCK1 and 2 act redundantly in regulating cell proliferation and their depletion causes cellular senescence.

A comprehensive molecular description of the cellular transition into replicative senescence provides evidence of metabolic, epigenetic, and regulatory rewiring that links senescence with wound healing and fibrosis.

Under metabolic syndrome, joint subchondral preosteoclasts acquire a senescence-associated secretome, which causes a rapid structural alteration of subchondral bone and contributes to the development of osteoarthritis.

Senescent cells are recurrently induced during limb regeneration in salamanders and subsequently eliminated by a highly efficient mechanism of macrophage-dependent surveillance.

Targeting senescent cells in human intervertebral discs, using senotherapeutics, provides a potential therapeutic strategy to prevent or reduce disc degeneration and pain.

The study of embryo-endometrial interactions in assembloid co-cultures identifies novel mechanisms of reproductive failure.