Heme induces programmed necrosis on macrophages through autocrine TNF and ROS production

TL;DR: Human aortic smooth muscle cells were selected as a model cell and it was demonstrated that heme triggers ER stress in a time- and dose-dependent manner in HAoSMCs, supporting their use as a potential therapeutic approach to reverse such a deleterious effects of heme toxicity.

TL;DR: In this paper, while atherosclerosis is an almost inevitable consequence of aging, food preferences, lack of exercise, and other aspects of the lifestyle in many countries, the identification of new

TL;DR: It is identified that the pro-oxidant, and not the proinflammatory, actions of heme profoundly impact on iron homeostasis by critically regulating the expression of ferroportin and iron export in hemolytic conditions.

TL;DR: It is demonstrated that renal hepcidin synthesis protects the DN against hemin and hemoglobin-mediated injury and prevents necroptosis.

TL;DR: This review will focus on the JNK group of MAP kinases, which are characterized by the sequence TEY and the two stress-activatedMAP kinases: p38 with the sequence TGY, and the c-Jun NH2-terminal kinases (JNK) with the sequences TPY.

TL;DR: The findings suggest that RIP3 controls programmed necrosis by initiating the pronecrotic kinase cascade, and that this is necessary for the inflammatory response against virus infections.

TL;DR: Evidence now reveals that necrosis can also occur in a regulated manner, and necroptosis participates in the pathogenesis of diseases, including ischaemic injury, neurodegeneration and viral infection, thereby representing an attractive target for the avoidance of unwarranted cell death.

TL;DR: Data indicate RIP3 as the determinant for cellular necrosis in response to TNF-alpha family of death-inducing cytokines.