Abstract
Osteoarthritis (OA) is traditionally considered an age-related disease. Therefore, repurposing drugs with the potential to reduce cell senescence is a justified therapeutic strategy. Such is the case of metformin, the most widely used antidiabetic medicine with well-known pharmacokinetics, acceptable toxicity, and beneficial metabolic effects. Metformin could significantly impact processes associated with aging and OA such as cellular senescence, infammaging, mitochondrial dysfunction and impaired nutrient sensing. The aim of the present narrative review is to unveil the potential of metformin to modify disease course in light of aging osteoarthritic joints. The drug has pleiotropic effects on chondrocyte and extracellular matrix metabolism and may provide through AMPK-dependent and -independent pathways a meaningful improvement of OA. Mostly preclinical and retrospective cohort studies have shown that metformin exposure could lead to the regulation of cartilage homeostasis, symptomatic relief of pain and postpone surgery for those suffering from OA. Randomized control trials are warranted to justify the preliminary expectations.
Publisher
Medical Center "Edem Medical" LLC