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RIP3: a molecular switch for necrosis and inflammation.

TLDR
The current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases is reviewed.
Abstract
The receptor-interacting protein kinase 3 (RIP3/RIPK3) has emerged as a critical regulator of programmed necrosis/ necroptosis, an inflammatory form of cell death with important functions in pathogen-induced and sterile inflammation. RIP3 activation is tightly regulated by phosphorylation, ubiquitination, and caspase-mediated cleavage. These post-translational modifications coordinately regulate the assembly of a macromolecular signaling complex termed the necrosome. Recently, several reports indicate that RIP3 can promote inflammation independent of its pronecrotic activity. Here, we review our current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases.

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Cell Death Pathways in Ischemic Stroke and Targeted Pharmacotherapy.

TL;DR: Understanding the role of different cell death pathways is crucial to aid in the modern treatment of protecting apoptotic neurons and considers investigation on non-classical pathways that are tightly regulated, may or may not involve caspases, but non-apoptotic.
Journal ArticleDOI

Retinal damage induced by commercial light emitting diodes (LEDs).

TL;DR: The role of blue light from LEDs in retinal damage was elucidated and LED light caused a state of suffering of the retina with oxidative damage and retinal injury.
Journal ArticleDOI

Inflammatory outcomes of apoptosis, necrosis and necroptosis.

TL;DR: The inflammatory implications of necrosis, necroptosis and apoptosis are discussed and some of the unresolved questions concerning how dead cells influence inflammatory responses are discussed.
Journal ArticleDOI

Necroptosis, in vivo detection in experimental disease models.

TL;DR: This review will present the last methodological advances for in vivo necroptosis identification and discuss past and recent data to provide an update of the so-called "necroptotic-associated pathologies".
References
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TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
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Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics.

TL;DR: Apoptosis seems to be involved in cell turnover in many healthy adult tissues and is responsible for focal elimination of cells during normal embryonic development, and participates in at least some types of therapeutically induced tumour regression.
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Cancer-related inflammation.

TL;DR: The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment.
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An endotoxin-induced serum factor that causes necrosis of tumors

TL;DR: It is proposed that TNF mediates endotoxin-induced tumor necrosis, and that it may be responsible for the suppression of transformed cells by activated macrophages.
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Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death

TL;DR: In this article, the authors found that doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin.
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