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Open AccessJournal ArticleDOI

Programmed cell death and its role in inflammation

TLDR
An overview of the major types of cell death related to inflammation is provided and modified cell death pathways are likely to be a logical therapeutic target for inflammatory diseases.
Abstract
Cell death plays an important role in the regulation of inflammation and may be the result of inflammation. The maintenance of tissue homeostasis necessitates both the recognition and removal of invading microbial pathogens as well as the clearance of dying cells. In the past few decades, emerging knowledge on cell death and inflammation has enriched our molecular understanding of the signaling pathways that mediate various programs of cell death and multiple types of inflammatory responses. This review provides an overview of the major types of cell death related to inflammation. Modification of cell death pathways is likely to be a logical therapeutic target for inflammatory diseases.

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Pyroptosis: A new frontier in cancer.

TL;DR: The mechanism of regulating pyroptosis in tumor cells as well as the potential roles of pyroPTosis in cancer are focused on to explore potential diagnostic markers in cancers contributing to the prevention and treatment in cancers.
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Pathogenesis of Nonalcoholic Steatohepatitis

TL;DR: Differences in these wound-healing responses among individuals determine whether lipotoxic livers regenerate, leading to stabilization or resolution of NASH, or develop progressive scarring, cirrhosis, and possibly liver cancer.
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The diverse origins of circulating cell-free DNA in the human body: a critical re-evaluation of the literature

TL;DR: This review presents an extensive compilation of the putative origins ofcfDNA and contrasts the contributions of cellular breakdown processes with active mechanisms for the release of cfDNA into the extracellular environment.
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Regulation of alveolar macrophage death in acute lung inflammation.

TL;DR: This review will focus on recent advances in the regulation and underlying mechanisms of AM death as well as the influence ofAM death on the development of ALI.
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Cell death mechanisms in eukaryotes

TL;DR: There are a number of cell deaths—some of them bearing a resemblance to apoptosis and/or necrosis, and many, distinct from each—that serve a multitude of roles in either supporting or disrupting the homoeostasis.
References
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Journal ArticleDOI

Neutrophil extracellular traps kill bacteria

TL;DR: It is described that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria, which degrade virulence factors and kill bacteria.
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Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-beta, PGE2, and PAF.

TL;DR: The results suggest that binding and/or phagocytosis of apoptotic cells induces active antiinflammatory or suppressive properties in human macrophages, likely that resolution of inflammation depends not only on the removal of apoptosis but on active suppression of inflammatory mediator production.
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Early redistribution of plasma membrane phosphatidylserine is a general feature of apoptosis regardless of the initiating stimulus: inhibition by overexpression of Bcl-2 and Abl.

TL;DR: It is shown that PS externalization is an early and widespread event during apoptosis of a variety of murine and human cell types, regardless of the initiating stimulus, and precedes several other events normally associated with this mode of cell death.
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NOX enzymes and the biology of reactive oxygen

TL;DR: Professional phagocytes generate high levels of reactive oxygen species (ROS) using a superoxide-generating NADPH oxidase as part of their armoury of microbicidal mechanisms, leading to the concept that ROS are 'intentionally' generated in these cells with distinctive cellular functions related to innate immunity, signal transduction and modification of the extracellular matrix.
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