Purpose of review: The concept of cellular senescence has been evolving. Although originally proposed based on studies of serum-driven replication of cell lines in vitro, it is now clear that cellular senescence occurs in vivo. It has also become clear that cellular senescence can be triggered by a number of stimuli such as radiation, chemotherapy, activation of oncogenes, metabolic derangements, and chronic inflammation.
Recent findings: As we learn more about the mechanisms of cellular aging, it has become important to ask whether accelerated cellular senescence occurs in lupus and other systemic rheumatologic diseases. Accelerated cellular aging may be one explanation for some of the excess morbidity and mortality seen in lupus patients. If so, drugs targeting cellular senescence may provide new options for preventing long-term complications such as organ failure in systemic lupus erythematosus patients.
Keywords: Cellular senescence; DNA damage; Mesenchymal stem cells; Systemic lupus erythematosus; Telomeres.