Autophagy in the Cellular Consequences of Tobacco Smoking: Insights into Senescence

Abstract

Smoking is a significant contributing factor to the development of many complex diseases. One of the most important stimuli for aging in the human body is constant exposure to environmental factors such as cigarette smoke. Free radicals in cigarette smoke cause reactive oxygen species production at the cellular level and induce inflammatory responses. The respiratory system of smokers exhibits age-related characteristics, such as enhanced oxidative stress, accumulated damaged proteins, and increased inflammation. Autophagy is triggered by tobacco smoke as a protective mechanism to prevent and reduce molecular stress. However, smoking can interfere with the normal functioning of autophagy in various ways. Smoking-induced impairment of autophagy leads to irreversible cellular damage accumulation, causing cells to undergo cellular aging or senescence. Senescent cells lose their ability to divide and display a distinct secretory phenotype called the senescence-associated secretory phenotype (SASP) and produce numerous growth factors, immune modulators, and inflammatory cytokines. This review discusses the effects of tobacco smoke exposure on autophagy alteration, cellular aging, and senescence induction in exposed animal models, as well as in exposed epithelial and immune cells in the body.