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portada Cellular Redox Mechanisms in Inflammation and Programmed Cell Death
Type
Physical Book
Publisher
Author
Language
English
Pages
230
Format
Hardcover
Dimensions
24.4x17x1.9 cm
ISBN13
9783725865307

Cellular Redox Mechanisms in Inflammation and Programmed Cell Death

Vlasova, Irina I. (Author) · Mdpi AG · Hardcover

Cellular Redox Mechanisms in Inflammation and Programmed Cell Death - Vlasova, Irina I.

New Book Imported to New Zealand
Delivery: 21 Oct - 28 Oct Shipping: 6 to 7 business days.
NZ$ 187.82
Import costs and 15% GST included in the price ✅
NZ$ 187.82

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Synopsis "Cellular Redox Mechanisms in Inflammation and Programmed Cell Death"

Redox reactions play an important role in the regulation of various physiological processes, resulting in the diversity of articles featured in this Special Issue (SI), from works studying mechanisms of antioxidant activity to a prospective randomized study of the effects of hypoxia-hyperoxia exposures on metabolic products of the intestinal microbiome in patients. In vitro, microbiota metabolites formed under inflammation and sepsis inhibit cyclooxygenase peroxidase activity. Macrophages are the most persistent cells at inflammatory sites, with phenotypes differing not only in cytokine secretion but also in the production of reactive oxygen species (ROS). Neuronal dysfunction and pain may be caused by an imbalance in ROS/reactive nitrogen species (RNS) and antioxidant defense; thus, compounds with antioxidant properties can be promising therapeutic agents to mitigate oxidative stress and alleviate pathological conditions. An example of this is manganese porphyrins, which target key pathways involved in neuropathic pain. In this SI, flavonoids, polyphenols, and selenium compounds are studied for their protective ability against inflammation and oxidative injury. Pre-treatment with ferroptosis inhibitors or maintenance of mitochondrial functions enables the safe rewarming of cooled cells. In contrast, excess glutamate triggers a cascade of oxidative and metabolic disorders causing neuronal ferroptosis, with mitochondria playing a central role in this vulnerability. While diverse in biological models, the articles in this SI all demonstrate that ROS/RNS disorder is both a driver of pathology and a target for therapeutic intervention.

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