Brooke T. Mossman

TL;DR: It is shown that asbestos and silica are sensed by the Nalp3 inflammasome, whose subsequent activation leads to interleukin-1β secretion, and support its role as a major proinflammatory “danger” receptor in particulate matter–related pulmonary diseases.

TL;DR: Some of the recent findings that illuminate the significance of redox signaling and exciting future perspectives are reviewed to highlight some of the current pitfalls and the approaches needed to advance this important area of biochemical and biomedical research.

TL;DR: The findings provide a mechanistic rationale for the paradoxical inability of asbestos to transform HM in vitro, elucidate and underscore the role of TNF-α in asbestos pathogenesis in humans, and identify potential molecular targets for anti-MM prevention and therapy.

TL;DR: There is strong evidence supporting the premise that oxidants contribute to asbestos-induced lung injury; thus, strategies for reducing oxidant stress to pulmonary cells may attenuate the deleterious effects of asbestos.

TL;DR: The results suggest that the geometry of particulates is of critical importance in the generation of O2-.