Aging is a natural process that causes physiological, morphological, and biochemical changes in tissues and organs, with a progressive decline in cellular functions. The main causes of diseases associated with aging, such as neurodegeneration, cancer, chronic inflammation, cardiovascular disease, and musculoskeletal disorders, can be traced to mechanisms of genetic instability, loss of protein homeostasis, and cellular senescence. In the context of the musculoskeletal system, aging is often associated with structural changes at the bone, joint, and muscle levels, contributing to the acceleration of the degenerative process of osteoarthritis (OA), one of the most prevalent degenerative joint diseases. Physical activity is essential for maintaining musculoskeletal function and promoting healthy aging. Irisin (Ir), a myokine released during muscle contraction, has been shown to exert beneficial effects, including enhancement of metabolic processes and stimulation of thermogenesis. Preliminary in vitro studies confirm that Ir can reduce cellular senescence and improve mitochondrial dynamics in chondrocytes, counteracting the deleterious effects of advanced glycation end-products (AGEs).
In this context, we hypothesize that physical exercise and Ir-based treatment may mitigate cartilage deterioration and systemic decline, thereby slowing the degenerative process and cellular senescence. The primary objective is to elucidate the molecular mechanisms underlying Ir activity in the SAMP8 (Senescence-Accelerated Mouse Prone 8) murine model, which undergoes early and rapid aging, making it a suitable system for studying age-related pathologies.