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Pulmonary fibrosis induced by repetitive chemical injury in mice involves cross talk among macrophages, endothelial cells and fibroblasts. Macrophages induce expression of the Notch ligand Jag1 in pulmonary capillary endothelial cells, leading to Notch pathway activation in perivascular fibroblasts and fibrosis.
Blocking the enzyme KMO with a small molecule reduces the levels of toxic tryptophan metabolites and reduces multiple extrapancreatic organ failure in a rat model of acute pancreatitis.
Reducing levels of mitochondrial iron by diet or pharmacological chelation ameliorates symptoms of cigarette smoke–induced chronic obstructive pulmonary disease in mice.
Judy Lieberman and colleagues show that intracellular parasites are eradicated by lymphocyte delivery of cytotoxic granule contents—perforin, granulysin and granzymes—into infected cells.
Myocardial injury induced by ischemia-reperfusion or doxorubicin leads to cardiomyocyte necroptosis via RIP3-mediated phosphorylation of CaMKII and opening of the mitochondrial permeability transition pore.