Molecular Responses to Asbestos: Induction of Cell Proliferation and Apoptosis Through Modulation of Redox-Dependent Cell Signaling Pathways
This chapter discusses how asbestos interacts with cell-signaling pathways to modulate cell functions, including induction of proliferation and cell death, either by necrosis or by apoptosis (programmed cell death). Activation of extracellular signal-regulated kinase (ERK) and other signaling pathways by asbestos, or reactive oxygen species/reactive nitrogen species (ROS/RNS) elaborated by asbestos, may be critical to elicitation of injury and proliferation in mesothelial and epithelial cells during carcinogenesis. The responses to asbestos are dose-related, and represent a dynamic balance between the induction of cell injury and cell death and promotion of cell proliferation. Chronic cell injury coupled with inflammatory responses also may promote compensatory hyperplasia over time. Because of its durability and capability to produce or modulate ROS/RNS, asbestos may have a unique ability to perturb cell signaling pathways.
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