What is necrosis?

from For the sake of reproducibility - a technical replicate by Tumor Necrosis Factor-alpha

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Necrosis, long thought to be a passive and otherwise chaotic cellular process
Cellular swelling, membrane rupture, loss of intracellular contents
The result of physico-chemical stress, hypoxia, IR, metabolism impairment

It appears that necrosis could be a much more well-orchestrated type of cell death
Precise execution mechanism, signal transduction pathways
Involved in particular developmental process, tissular homeostasis

Ischemia – inadequate oxygen and nutrient supply
Reperfusion – increased cell death following bloodflow restoration
Oxphos inhibition – intracellular ATP depletion
A switch from apoptosis – to necrosis in the presence of apoptotic signalization

Induction of necrosis by ligand-death receptor interaction
TRAIL, Fas, TNFR1, requiring translational inhibition
Blocked caspases, apoptosis prevented, necrotic death initiation

Inflammatory response initiation lead by various pathogen recognition receptors
Exogenous lipopolysaccharide, bacterial RNA, peptidoglycans
Triggering necrotic cell death in various murine and human cellular lineages

Reactive oxygen species – damages resulting in mitochondrial dysfunction
RIP1 – TNF-dependent mitochondrial (re)localization
Immune recognition – phosphatidylserine externalization
Macrophages – necrotic cell clearance by phagocytic engulfment

Ref: Vanlangenakker N et al. “Molecular mechanisms and pathophysiology of necrotic cell death.” Current Molecular Medicine 8(3):207-220. (2008)

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from For the sake of reproducibility - a technical replicate, released January 24, 2018

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Tumor Necrosis Factor-alpha Neuville, Québec

Scientists, academics, gorefiends and grindheads of the world rejoice: Tumor Necrosis Factor-alpha unleashes its take on full blown Carcass-worship, topped with unique lyrical themes inspired by the most recent knowledge in state-of-the-art scientific research from the fields of cellular and molecular biology. ... more

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