Cheryl L. Fattman

TL;DR: MSCs protect lung tissue from BLM-induced injury by blocking TNF-α and IL-1, two fundamental proinflammatory cytokines in lung, which may provide a novel cellular vector for treating chronic inflammatory diseases in humans.

TL;DR: This review will discuss the regulation of EC-SOD and its role in a variety of oxidant-mediated diseases.

TL;DR: Investigation into therapeutic approaches to inhibit oxidant-mediated reactions in the initiation and progression of pulmonary fibrosis may provide hope for the future treatment of this disease.

TL;DR: Data from studies on mouse models of pulmonary fibrosis and human IPF tissues indicate that loss of RAGE contributes to IPF pathogenesis, and immunohistochemical and hydroxyproline quantification studies on aged RAGE-null mice indicate that these mice spontaneously developmonary fibrosis-like alterations.

TL;DR: It is demonstrated that, in addition to binding heparin, EC-SOD specifically binds to type I collagen with a dissociation constant (Kd) of 200 nm, and the heparIn-binding region was found to mediate the interaction with collagen.