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Open AccessJournal ArticleDOI

Necroptosis: The Release of Damage-Associated Molecular Patterns and Its Physiological Relevance

Agnieszka Kaczmarek, +2 more
- 21 Feb 2013 - 
- Vol. 38, Iss: 2, pp 209-223
TLDR
The physiological relevance of necroptosis and its role in the modulation of inflammation are discussed and apparently immunologically silent maintenance of T cell homeostasis is investigated.
About
This article is published in Immunity.The article was published on 2013-02-21 and is currently open access. It has received 1081 citations till now. The article focuses on the topics: Necroptosis & RIPK1.

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Citations
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Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Lorenzo Galluzzi, +186 more
TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
Journal ArticleDOI

Necroptosis and its role in inflammation

TL;DR: The mechanisms regulating necroptosis and its potential role in inflammation and disease are discussed and RIPK1 has important kinase-dependent and scaffolding functions that inhibit or trigger necroPTosis and apoptosis.
Journal ArticleDOI

Regulated necrosis: the expanding network of non-apoptotic cell death pathways

TL;DR: Elucidating how these pathways of regulated necrosis are interconnected at the molecular level should enable this process to be therapeutically targeted.
References
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Journal ArticleDOI

Pattern Recognition Receptors and Inflammation

TL;DR: The role of PRRs, their signaling pathways, and how they control inflammatory responses are discussed.
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Release of chromatin protein HMGB1 by necrotic cells triggers inflammation

TL;DR: It is reported that Hmgb1-/- necrotic cells have a greatly reduced ability to promote inflammation, which proves that the release of HMGB1 can signal the demise of a cell to its neighbours, and cells undergoing apoptosis are programmed to withhold the signal that is broadcast by cells that have been damaged or killed by trauma.
Journal ArticleDOI

Circulating mitochondrial DAMPs cause inflammatory responses to injury

TL;DR: It is shown that injury releases mitochondrial DAMPs into the circulation with functionally important immune consequences, including formyl peptides and mitochondrial DNA, which promote PMN Ca2+ flux and phosphorylation of mitogen-activated protein (MAP) kinases, thus leading to PMN migration and degranulation in vitro and in vivo.
Journal ArticleDOI

Mechanisms of mitophagy

TL;DR: Mitophagy, the specific autophagic elimination of mitochondria, has been identified in yeast, and in mammals during red blood cell differentiation, mediated by NIP3-like protein X (NIX; also known as BNIP3L).
Journal ArticleDOI

Sterile inflammation: sensing and reacting to damage

TL;DR: The triggers and receptor pathways that result in sterile inflammation and its impact on human health are reviewed.
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