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Arachidonic Acid as a Key Inflammatory Intermediate: Metabolic Pathways and Potential Therapeutic Targets

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Bioactive Lipids".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 7420

Special Issue Editors

Dr. Rashika El Ridi

E-Mail Website
Guest Editor
Zoology Department, Faculty of Science, Cairo University, Giza, Egypt
Interests: vaccines; drugs; schistosomiasis; antibodies; immunity; PCR; cloning; immunology of infectious diseases; innate immunity; parasites and cancer immune evasion
Dr. Wen Wang Dao

E-Mail Website
Guest Editor
Department of Cardiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Interests: hypertension; fulminant myocarditis; genetic diagnosis; personalized medicine

Special Issue Information

Dear Colleagues,

Arachidonic acid is now at the center of industrial and economic interests due to increased awareness of its importance for the optimal growth and development of the fetus and infants, the health of adults, and the cognitive powers of the elderly. Eminent contributors are herein invited to clarify the basis of the importance of arachidonic acid consumption, especially in developing countries, and delineate user-friendly procedures for its commercial production.

Arachidonic acid’s different metabolic pathways are intricate, and accordingly, we need contributions that explain, clarify and simplify each metabolic step to encourage the development of drugs and strategies for maximizing this critical nutrient’s benefits and eliminating any potential harm.

Arachidonic acid is present at the heart of raging controversies regarding its role in eliciting and resolving inflammation, cancer cell initiation and apoptosis, and the induction and alleviation of neurological disorders. Accordingly, we invite eminent contributors to this Special Issue to provide the necessary arguments and evidence for refuting or supporting arachidonic acid’s pathologic or beneficial roles in cancer, metabolic disorders (especially diabetes), and afflictions of the muscle, immune and nervous systems.

Dr. Rashika El Ridi
Dr. Wen Wang Dao
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Molecules is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • arachidonic acid production
  • arachidonic acid pathways
  • arachidonic acid metabolites and inflammation
  • resolvins
  • arachidonic acid and cancer
  • sphingomyelin
  • arachidonic acid deficiency

Published Papers (3 papers)

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Research

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17 pages, 21050 KiB  
Article
Mechanisms of Arachidonic Acid In Vitro Tumoricidal Impact
by Hatem Tallima and Rashika El Ridi
Molecules 2023, 28(4), 1727; https://doi.org/10.3390/molecules28041727 - 11 Feb 2023
Cited by 2 | Viewed by 1371
Abstract
To promote the potential of arachidonic acid (ARA) for cancer prevention and management, experiments were implemented to disclose the mechanisms of its tumoricidal action. Hepatocellular, lung, and breast carcinoma and normal hepatocytes cell lines were exposed to 0 or 50 μM ARA for [...] Read more.
To promote the potential of arachidonic acid (ARA) for cancer prevention and management, experiments were implemented to disclose the mechanisms of its tumoricidal action. Hepatocellular, lung, and breast carcinoma and normal hepatocytes cell lines were exposed to 0 or 50 μM ARA for 30 min and then assessed for proliferative capacity, surface membrane-associated sphingomyelin (SM) content, neutral sphingomyelinase (nSMase) activity, beta 2 microglobulin (β2 m) expression, and ceramide (Cer) levels. Reactive oxygen species (ROS) content and caspase 3/7 activity were evaluated. Exposure to ARA for 30 min led to impairment of the tumor cells’ proliferative capacity and revealed that the different cell lines display remarkably similar surface membrane SM content but diverse responses to ARA treatment. Arachidonic acid tumoricidal impact was shown to be associated with nSMase activation, exposure of cell surface membrane β2 m to antibody binding, and hydrolysis of SM to Cer, which accumulated on the cell surface and in the cytosol. The ARA and Cer-mediated inhibition of tumor cell viability appeared to be independent of ROS generation or caspase 3/7 activation. The data were compared and contrasted to findings reported in the literature on ARA tumoricidal mechanisms. Full article
(This article belongs to the Special Issue Arachidonic Acid as a Key Inflammatory Intermediate: Metabolic Pathways and Potential Therapeutic Targets)
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Review

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25 pages, 2928 KiB  
Review
Crosstalk between Depression and Breast Cancer via Hepatic Epoxide Metabolism: A Central Comorbidity Mechanism
by Zhen Ye, Kumar Ganesan, Mingquan Wu, Yu Hu, Yingqi She, Qianqian Tian, Qiaobo Ye and Jianping Chen
Molecules 2022, 27(21), 7269; https://doi.org/10.3390/molecules27217269 - 31 Oct 2022
Cited by 1 | Viewed by 1973
Abstract
Breast cancer (BC) is a serious global challenge, and depression is one of the risk factors and comorbidities of BC. Recently, the research on the comorbidity of BC and depression has focused on the dysfunction of the hypothalamic–pituitary–adrenal axis and the persistent stimulation [...] Read more.
Breast cancer (BC) is a serious global challenge, and depression is one of the risk factors and comorbidities of BC. Recently, the research on the comorbidity of BC and depression has focused on the dysfunction of the hypothalamic–pituitary–adrenal axis and the persistent stimulation of the inflammatory response. However, the further mechanisms for comorbidity remain unclear. Epoxide metabolism has been shown to have a regulatory function in the comorbid mechanism with scattered reports. Hence, this article reviews the role of epoxide metabolism in depression and BC. The comprehensive review discloses the imbalance in epoxide metabolism and its downstream effect shared by BC and depression, including overexpression of inflammation, upregulation of toxic diols, and disturbed lipid metabolism. These downstream effects are mainly involved in the construction of the breast malignancy microenvironment through liver regulation. This finding provides new clues on the mechanism of BC and depression comorbidity, suggesting in particular a potential relationship between the liver and BC, and provides potential evidence of comorbidity for subsequent studies on the pathological mechanism. Full article
(This article belongs to the Special Issue Arachidonic Acid as a Key Inflammatory Intermediate: Metabolic Pathways and Potential Therapeutic Targets)
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24 pages, 4419 KiB  
Review
CYP450 Epoxygenase Metabolites, Epoxyeicosatrienoic Acids, as Novel Anti-Inflammatory Mediators
by Zeqi Shi, Zuowen He and Dao Wen Wang
Molecules 2022, 27(12), 3873; https://doi.org/10.3390/molecules27123873 - 16 Jun 2022
Cited by 18 | Viewed by 3372
Abstract
Inflammation plays a crucial role in the initiation and development of a wide range of systemic illnesses. Epoxyeicosatrienoic acids (EETs) are derived from arachidonic acid (AA) metabolized by CYP450 epoxygenase (CYP450) and are subsequently hydrolyzed by soluble epoxide hydrolase (sEH) to dihydroxyeicosatrienoic acids [...] Read more.
Inflammation plays a crucial role in the initiation and development of a wide range of systemic illnesses. Epoxyeicosatrienoic acids (EETs) are derived from arachidonic acid (AA) metabolized by CYP450 epoxygenase (CYP450) and are subsequently hydrolyzed by soluble epoxide hydrolase (sEH) to dihydroxyeicosatrienoic acids (DHETs), which are merely biologically active. EETs possess a wide range of established protective effects on many systems of which anti-inflammatory actions have gained great interest. EETs attenuate vascular inflammation and remodeling by inhibiting activation of endothelial cells and reducing cross-talk between inflammatory cells and blood vessels. EETs also process direct and indirect anti-inflammatory properties in the myocardium and therefore alleviate inflammatory cardiomyopathy and cardiac remodeling. Moreover, emerging studies show the substantial roles of EETs in relieving inflammation under other pathophysiological environments, such as diabetes, sepsis, lung injuries, neurodegenerative disease, hepatic diseases, kidney injury, and arthritis. Furthermore, pharmacological manipulations of the AA-CYP450-EETs-sEH pathway have demonstrated a contribution to the alleviation of numerous inflammatory diseases, which highlight a therapeutic potential of drugs targeting this pathway. This review summarizes the progress of AA-CYP450-EETs-sEH pathway in regulation of inflammation under different pathological conditions and discusses the existing challenges and future direction of this research field. Full article
(This article belongs to the Special Issue Arachidonic Acid as a Key Inflammatory Intermediate: Metabolic Pathways and Potential Therapeutic Targets)
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