Eicosanoids in inflammation: biosynthesis, pharmacology, and therapeutic frontiers.

doi:10.2174/156802607779941314

Paper

Eicosanoids in inflammation: biosynthesis, pharmacology, and therapeutic frontiers.

Published Jan 31, 2007 · S. Khanapure, D. Garvey, D. Janero

Current topics in medicinal chemistry

Q2 SJR score

326

Citations

7

Influential Citations

Full textSemantic Scholar

Abstract

In mammalian cells, eicosanoid biosynthesis is usually initiated by the activation of phospholipase A2 and the release of arachidonic acid (AA) from membrane phospholipids. The AA is subsequently transformed by cyclooxygenase (COX) and lipoxygenase (LO) pathways to prostaglandins, thromboxane and leukotrienes collectively termed eicosanoids. Eicosanoid production is considerably increased during inflammation. Both COX and LO pathways are of particular clinical relevance. The COX pathway is the major target for non-steroidal anti-inflammatory drugs (NSAIDs), the most popular medications used to treat pain, fever and inflammation. Although their anti-inflammatory effects are well known, their long-term use is associated with gastrointestinal (GI) complications such as ulceration. In 1991, it was discovered that COX exists in two distinct isozymes, COX-1 and COX-2, of which COX-2 is primarily expressed at sites of inflammation and produces pro-inflammatory eicosanoids. For this reason, COX-2 selective inhibitors (COXIBs) have been developed recently as anti-inflammatory agents to minimize the risk of GI toxicity. Recently, some COX-2 selective inhibitors have shown adverse cardiovascular side effects, resulting in the withdrawal of rofecoxib and valdecoxib from the market. Selective inhibition of COX-2 without reducing COX-1-mediated thromboxane production could alter the balance between prostacyclin and thromboxane and promote a prothrombotic state, thereby explaining the observed COX-2 cardiovascular risk. In this review, we describe mechanisms for the production of pro-inflammatory eicosanoid mediators contributing to inflammation and summarize promising options for the prevention of inflammatory mediator formation and the therapeutic inhibition of pain and inflammation.

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Study Snapshot

Eicosanoids play a crucial role in inflammation, and targeting COX-2 may help prevent inflammatory mediator formation and inhibit pain and inflammation without causing cardiovascular side effects.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Eicosanoids in inflammation: biosynthesis, pharmacology, and therapeutic frontiers.

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References

Citations

The Octadecanoids: Synthesis and Bioactivity of 18-Carbon Oxygenated Fatty Acids in Mammals, Bacteria, and Fungi

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The cardioprotective effects of polyunsaturated fatty acids depend on the balance between their anti-inflammatory and pro-oxidative properties, with n-3 PUFAs being more effective than n-6 FAs.

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Higher levels of unsaturated fatty acids like n-3 PUFA and MUFA may reduce pancreatic cancer risk, while higher levels of n-6 polyunsaturated fatty acids and saturated fatty acids increase it.

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Understanding cancer metabolism and nutrition-based interventions is crucial for developing more effective cancer prevention and treatment strategies.

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Controlling inflammatory mediators in dental pulp inflammation may lead to healing and preservation of pulp tissue.

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Malassezia yeasts on the skin can produce lipid mediators that reduce redness and itching associated with inflammatory skin conditions, offering potential for new cosmetic and therapeutic solutions.

IL-13 decreases susceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo

IL-13 protects airway epithelial cells from SARS-CoV-2 infection in vitro but worsens disease severity in vivo, suggesting that targeting IL-13 and eicosanoid signaling may help protect against severe respiratory virus-induced lung diseases.