ABSTRACT
Apoptosis plays a major role in homeostasis to maintain a balance between cell survival and death, and is involved in the pathophysiology of various lung diseases. Lung epithelium and endothelium are not only the primary site of lung damage but also participates in infl ammatory reaction through a number of mechanisms, including the release of infl ammatory mediators and reactive oxygen species. Apoptosis signaling is classically composed of two principal pathways. One is a direct pathway from death receptor ligation to caspase cascade activation and apoptosis. Th e other pathway triggered by stresses such as drugs, radiation, infectious agents and reactive oxygen species is mediated by mitochondria. Endoplasmic reticulum is also shown to be the organelle to mediate apoptosis. Apoptosis is followed by remodeling processes, which consist of epithelial, endothelial, and fi broblast activation, infl ammation, oxidative stress, protease activation, coagulation pathway activation, neoangiogenesis, re-epithelialization, and fi brosis. Parenchymal and mesenchymal interaction plays important roles in these processes. As well as parenchymal cell apoptosis, infl ammatory cell apoptosis has important roles in the resolution of infl ammation, and is involved in the pathogenesis of lung diseases. Further understanding of apoptosis signaling and
its regulation by novel strategies may lead to eff ective treatments against various lung diseases.
