The Cellular Senescence Program

Abstract

Mitosis is the process of somatic cell division that governs development of all organs in the eukaryotic system. Somatic cell division occurs for about 60 doubling times under in vitro cultures, called the Hayflick limit, whereby the cells undergo cell cycle arrest [1]. In in vivo conditions, the cells also attain the finite level of division, a phenomenon called cellular senescence [2]. Cellular senescence could be classified into two types, irreversible and reversible, depending on the type of response the cells have undergone. Upon series of oxidative stress signals and mitogenic activation, the cells undergo irreversible arrest. These cells remain metabolically active but with altered protein expression profile. Therefore, irreversible cellular senescence is considered as a tumor suppressive mechanism. On the contrary, in reversible type of cellular senescence, oncogenic/mitogenic stimulation and telomere shortening elicit DNA damage response, and post cell cycle arrest, these cells undergo either apoptosis or revert back into transformed phenotypes. Under in vitro culture conditions, cellular senescence is classified as the replicative senescence and premature senescence, which correspond to the activation of DNA damage response signals and oxidative stress signals, respectively. In this chapter, we present a broad account of factors that contribute to cellular senescence and how senescent cells in turn contribute to aging and age-associated pathologies of the lungs. Characteristics of senescent cells and the inflammatory microenvironmentStudies on characteristics of senescence have covered in large using mesenchymal cell cultures under in vitro conditions. In recent years, epithelial cell senescence has emerged in age-related tissue damage. Phenotypically, the cells are distended with increased senescence-associated