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Review
. 2018 Sep;37(2-3):203-211.
doi: 10.1007/s10555-018-9741-1.

Stress, inflammation, and eicosanoids: an emerging perspective

Affiliations
Review

Stress, inflammation, and eicosanoids: an emerging perspective

Sujanitha Umamaheswaran et al. Cancer Metastasis Rev. 2018 Sep.

Abstract

Clinical and experimental studies support the notion that adrenergic stimulation and chronic stress affect inflammation, metabolism, and tumor growth. Eicosanoids are also known to heavily influence inflammation while regulating certain stress responses. However, additional work is needed to understand the full extent of interactions between the stress-related pathways and eicosanoids. Here, we review the potential influences that stress, inflammation, and metabolic pathways have on each other, in the context of eicosanoids. Understanding the intricacies of such interactions could provide insights on how systemic metabolic effects mediated by the stress pathways can be translated into therapies for cancer and other diseases.

Keywords: Cancer; Eicosanoids; Inflammation; PGE2; Stress.

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Figures

Fig. 1
Fig. 1
Biosynthesis of eicosanoids. Arachidonic acid metabolism is initiated by phospholipase A which is activated by various chemical and mechanical stimuli, leading to arachidonic acid generation. Free arachidonic acid is metabolized by two main enzymes, cyclooxygenases (COX), and lipoxygenases (LOX). COX enzymes (COX-1 and COX-2) catalyze the formation of PGH2, which is further converted to various prostanoids (prostaglandins, prostacyclins, and thromboxanes). LOX enzymes (5-LOX, 12-LOX, and 15-LOX) mediate the synthesis of leukotrienes, hydroxyeicosatetraenoic acid (HETE) and lipoxins
Fig. 2
Fig. 2
Stress and eicosanoids directly influence inflammation. However, the relationship between stress and eicosanoids is not well established. Eicosanoids activate certain components of CNS-mediated stress response pathway, while stress mediators are known to influence synthesis of certain eicosanoids. It is possible that stress mediators and eicosanoid-synthesizing enzymes influence each other, should their basal levels be disrupted. However, additional research is needed to elucidate the exact pathways and mediators involved in this interaction

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