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## What Causes Senescent Cells? Senescent cell accumulation can occur due to a variety of factors such as various age-related chronic diseases, oxidative stress, hormonal milieu, developmental factors, chronic infection (eg, human immunodeficiency virus [HIV]), certain medications (chemotherapy or certain HIV protease inhibitors), and radiation exposure. There are different types of cellular senescence that have been identified, including oncogene-induced senescence, stress-induced
What Causes Senescent Cells? Senescent cell accumulation can occur due to a variety of factors such as various age-related chronic diseases, oxidative stress, hormonal milieu, developmental factors, chronic infection (eg, human immunodeficiency virus [HIV]), certain medications (chemotherapy or certain HIV protease inhibitors), and radiation exposure. There are different types of cellular senescence that have been identified, including oncogene-induced senescence, stress-induced
“A significant increase in viral replication efficiency was detected by replicative senescence during IFV and VZV infection. ... As one of possible mechanisms for the increase in viral replication in senescent cells, a reduction in interferon (IFN) response after viral infection may account for it.” (2) **The concentration of this DNA virus in senescent cells is 300% more infected than non-senescent cells.**
## Senescent Cells (Zombie Cells) in the Lungs Constantly Secrete Inflammatory Cytokines, Worsening Diseases like COPD and Emphysema. **"Senescent cells increase the damage of neighboring cells by virtue of their SASP phenotype."** (1) "Inflammatory and structural cells (epithelial cells, endothelial cells, and fibroblasts) together contribute to incite inflammation and cellular senescence by secreting pro-inflammatory mediators, proteases, and lipid regulators in the lungs. This phenomen
## Inducing Senescence in Cancer Cells. "A substantial number of anticancer interventions induce senescence in cancer cells by triggering genotoxic stress, hyperactivation of mitogenic signalling or oxidative stress, leading to stable cell cycle arrest and SASP induction. Therefore, therapy-induced senescence serves as an initial antitumour mechanism to halt proliferation and prevent further genomic instability (Fig. 1). "