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

TL;DR: Methemoglobin peroxidase activity can be probed for subduing cellular toxicity of pro-oxidant molecules and it may in-turn make up for host immune response against the malaria parasite.

TL;DR: The mechanisms by which HO-1 expression is induced and how the enzyme regulates inflammatory and immune responses during infection with a number of different intracellular bacterial and protozoan pathogens are reviewed, highlighting mechanistic commonalities and differences with the goal of identifying targets for disease intervention.

TL;DR: Whether targeting a subset of the molecules shed by TACE, specifically those leading to TAMs with altered functions and phenotype, holds greater therapeutic promises than past clinical trials of TACE antagonists’ remains to be determined.

TL;DR: An increase of lipid level and later formation of lipid droplets during the erythrophagocytosis process inside RAW 264.7 macrophages and murine Kupffer cells is observed.

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.