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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.
A new study in mice suggests that pharmacologically targeting the apoptosis proteins BCL-2 and BCL-xL can clear senescent cells from bone marrow and ameliorate stem cell function during aging, bringing us a step closer to preventing senescence-associated tissue attrition in the clinic.
Sentinel macrophages in the lymph node provide a first line of defense against invading viruses. A new study visualizes inflammasome activation in virally infected nodal macrophages in mice and shows that this activation augments both innate and adaptive immunity.
A new study demonstrates that dysregulation of proteostasis can be a transforming event in hematopoiesis that could prove to be therapeutically actionable for treatment of myeloproliferative neoplasms.
A new study shows that aggregated forms of tau that cause frontotemporal dementia impair proteasome activity. Furthermore, proteasome inhibition can be alleviated by a small molecule that leads to proteasome phosphorylation and activation, thereby reducing tau accumulation.
Reproducibility projects yield headline-grabbing numbers, not practical steps for minimizing the investment in and publication of irreproducible research. If used inappropriately, these numbers may have unintended consequences.
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.