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Open AccessJournal ArticleDOI

Reactive Oxygen Species in Inflammation and Tissue Injury

TLDR
The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury.
Abstract
Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury.

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Citations
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Journal ArticleDOI

ROS Function in Redox Signaling and Oxidative Stress

TL;DR: It is argued that redox biology, rather than oxidative stress, underlies physiological and pathological conditions.
Journal ArticleDOI

ROS Are Good.

TL;DR: This Opinion focuses on the possibility that ROS are beneficial to plants, supporting cellular proliferation, physiological function, and viability, and that maintaining a basal level of ROS in cells is essential for life.
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Oxidative stress and reactive oxygen species in endothelial dysfunction associated with cardiovascular and metabolic diseases

TL;DR: This review will focus on the main mechanisms involved in the onset of endothelial dysfunction, with particular focus on inflammation and aberrant ROS production and on their relationship with classical and non-classical cardiovascular risk factors, such as hypertension, metabolic disorders, and aging.
Journal ArticleDOI

Does the Interdependence between Oxidative Stress and Inflammation Explain the Antioxidant Paradox

TL;DR: To examine whether the interdependence between oxidative stress and inflammation can explain the antioxidant paradox, the basic aspects of oxidative Stress and inflammation and their relationship and dependence are discussed.
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.
Journal ArticleDOI

Exploring the full spectrum of macrophage activation.

TL;DR: This Review suggests a new grouping of macrophages based on three different homeostatic activities — host defence, wound healing and immune regulation, and proposes that similarly to primary colours, these three basic macrophage populations can blend into various other 'shades' of activation.
Journal ArticleDOI

Pattern Recognition Receptors and Inflammation

TL;DR: The role of PRRs, their signaling pathways, and how they control inflammatory responses are discussed.
Journal ArticleDOI

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.
Journal ArticleDOI

Neutrophil recruitment and function in health and inflammation

TL;DR: The key features of the life of a neutrophil are discussed, from its release from bone marrow to its death, and the mechanisms that are used by neutrophils to promote protective or pathological immune responses at different sites are explained.
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