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Review
. 2018:228:63-86.
doi: 10.1007/978-3-319-68483-3_4.

Pulmonary Endothelial Cell Apoptosis in Emphysema and Acute Lung Injury

Eboni Chambers  1   2 , Sharon Rounds  1   2 , Qing Lu  3   4
Affiliations
Review

Pulmonary Endothelial Cell Apoptosis in Emphysema and Acute Lung Injury

Eboni Chambers et al. Adv Anat Embryol Cell Biol. 2018.

Abstract

Apoptosis plays an essential role in homeostasis and pathogenesis of a variety of human diseases. Endothelial cells are exposed to various environmental and internal stress and endothelial apoptosis is a pathophysiological consequence of these stimuli. Pulmonary endothelial cell apoptosis initiates or contributes to progression of a number of lung diseases. This chapter will focus on the current understanding of the role of pulmonary endothelial cell apoptosis in the development of emphysema and acute lung injury (ALI) and the factors controlling pulmonary endothelial life and death.

Keywords: ARDS; Acute lung injury; Apoptosis; Autophagy; COPD; ER stress; Emphysema; Endothelial cells; Necroptosis; Necrosis; Pulmonary; Unfolded protein response.

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Figures

Fig. 4.1
Fig. 4.1. Signaling pathways to CS-induced pulmonary endothelial cell apoptosis
Multiple signaling pathways are involved in CS-induced pulmonary endothelial cell apoptosis. (1) CS reduces VEGF/VEGFR2 signaling, leading to induction of ceramide and consequent apoptosis; (2) CS reduces FAK activation, leading to activation of p53 and inhibition of PI3K/Akt signaling, which results in apoptosis; (3) CS causes mitochondrial oxidative stress and mitochondrial dysfunction, leading to apoptosis; (4) CS elevates adenosine levels, leading to inactivation of Ras and mitochondrial oxidative stress, resulting in apoptosis; (5) CS impairs unfolded protein response, leading to apoptosis
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