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Review
. 2019 Jul 27;20(15):3683.
doi: 10.3390/ijms20153683.

Arachidonic Acid Metabolism and Kidney Inflammation

Tianqi Wang  1   2 , Xianjun Fu  2   3 , Qingfa Chen  4 , Jayanta Kumar Patra  5 , Dongdong Wang  6   7 , Zhenguo Wang  8 , Zhibo Gai  9
Affiliations
Review

Arachidonic Acid Metabolism and Kidney Inflammation

Tianqi Wang et al. Int J Mol Sci. .

Abstract

As a major component of cell membrane lipids, Arachidonic acid (AA), being a major component of the cell membrane lipid content, is mainly metabolized by three kinds of enzymes: cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP450) enzymes. Based on these three metabolic pathways, AA could be converted into various metabolites that trigger different inflammatory responses. In the kidney, prostaglandins (PG), thromboxane (Tx), leukotrienes (LTs) and hydroxyeicosatetraenoic acids (HETEs) are the major metabolites generated from AA. An increased level of prostaglandins (PGs), TxA2 and leukotriene B4 (LTB4) results in inflammatory damage to the kidney. Moreover, the LTB4-leukotriene B4 receptor 1 (BLT1) axis participates in the acute kidney injury via mediating the recruitment of renal neutrophils. In addition, AA can regulate renal ion transport through 19-hydroxystilbenetetraenoic acid (19-HETE) and 20-HETE, both of which are produced by cytochrome P450 monooxygenase. Epoxyeicosatrienoic acids (EETs) generated by the CYP450 enzyme also plays a paramount role in the kidney damage during the inflammation process. For example, 14 and 15-EET mitigated ischemia/reperfusion-caused renal tubular epithelial cell damage. Many drug candidates that target the AA metabolism pathways are being developed to treat kidney inflammation. These observations support an extraordinary interest in a wide range of studies on drug interventions aiming to control AA metabolism and kidney inflammation.

Keywords: arachidonic acid; cyclooxygenase; cytochrome P450; kidney inflammation; lipoxygenase; therapeutic target.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Scheme of eicosanoids biosynthesis pathways from arachidonic acid.
Figure 2
Figure 2
Lipoxygenase, and dehydrogenase pathways for the formation of HETEs, oxo-ETEs, and related eicosanoids.
See this image and copyright information in PMC

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