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Open AccessJournal ArticleDOI

Decoding cell death signals in liver inflammation.

TLDR
The cellular and molecular mechanisms that account for the most deleterious effect of hepatic inflammation at the cellular level are discussed, that is, the initiation of a massive cell death response among hepatocytes.
About
This article is published in Journal of Hepatology.The article was published on 2013-09-01 and is currently open access. It has received 696 citations till now. The article focuses on the topics: Innate immune system & Inflammation.

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Citations
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Inflammatory responses and inflammation-associated diseases in organs

TL;DR: Inflammation is a biological response of the immune system that can be triggered by a variety of factors, including pathogens, damaged cells and toxic compounds, potentially leading to tissue damage or disease.
Journal ArticleDOI

Immunological Effects of Conventional Chemotherapy and Targeted Anticancer Agents.

TL;DR: The tremendous clinical success of checkpoint blockers illustrates the potential of reestablishing latent immunosurveillance for cancer therapy, and their in-depth comprehension will facilitate the design of novel combinatorial regimens with improved clinical efficacy.
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Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Lorenzo Galluzzi, +121 more
TL;DR: The Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.
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Hepatic stellate cells as key target in liver fibrosis

TL;DR: Cell type- and target-specific pharmacological intervention to therapeutically induce the deactivation of hepatic stellate cells will enable more effective and less toxic precision antifibrotic therapies.
References
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Journal ArticleDOI

Free Radicals in the Physiological Control of Cell Function

Wulf Dröge
TL;DR: There is growing evidence that aging involves, in addition, progressive changes in free radical-mediated regulatory processes that result in altered gene expression.
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Inflammation and metabolic disorders

TL;DR: Dysfunction of the immune response and metabolic regulation interface can be viewed as a central homeostatic mechanism, dysfunction of which can lead to a cluster of chronic metabolic disorders, particularly obesity, type 2 diabetes and cardiovascular disease.
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Cleavage of BID by Caspase 8 Mediates the Mitochondrial Damage in the Fas Pathway of Apoptosis

TL;DR: The results indicate that BID is a mediator of mitochondrial damage induced by Casp8, and coexpression of BclxL inhibits all the apoptotic changes induced by tBID.
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Gout-associated uric acid crystals activate the NALP3 inflammasome

TL;DR: It is shown that MSU and CPPD engage the caspase-1-activating NALP3 (also called cryopyrin) inflammasome, resulting in the production of active interleukin (IL)-1β and IL-18 in mice deficient in the IL-1β receptor.
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A role for mitochondria in NLRP3 inflammasome activation

TL;DR: It is shown that mitophagy/autophagy blockade leads to the accumulation of damaged, ROS-generating mitochondria, and this in turn activates the NLRP3 inflammasome, and may explain the frequent association of mitochondrial damage with inflammatory diseases.
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