Cyp2c23 is a member of the cytochrome P450 2C subfamily. It functions as an arachidonic acid epoxygenase, converting arachidonic acid to epoxyeicosatrienoic acids (EETs) [3]. These EETs are involved in the regulation of renal vascular tone, salt excretion, and act as anti-inflammatory mediators, inhibiting nuclear factor-kappa B activation [4]. The gene is constitutively expressed in rat liver and kidney, with its expression showing age-and tissue-dependent patterns [1].

In rats, low Na intake downregulates the activity and expression of Cyp2c23, which in turn attenuates the inhibitory effect of arachidonic acid on epithelial Na channels (ENaC) and Na transport [2]. A peroxisome proliferator-activated receptor-alpha activator, fenofibrate, strongly induces renal Cyp2c23 protein and AA-epoxygenase activity, protecting against angiotensin II-induced renal damage [4]. Also, in a rodent model of septic shock, decreased expression and/or activity of soluble epoxide hydrolase and MEK1/ERK1/2/IKKβ/IκB-α/NF-κB pathway associated with increased Cyp2c23 expression and anti-inflammatory mediator formation participate in the protective effect of 5,14-HEDGE against hypotension, tachycardia, inflammation, and mortality [5]. In salt-sensitive hypertension in rats, tumor necrosis factor alpha contributes to the downregulation of Cyp2c23, blood pressure regulation, and renal injury, and blocking it increases Cyp2c23 expression and slows renal damage progression [6].

In conclusion, Cyp2c23 plays a crucial role in renal function regulation, especially in processes related to Na transport, blood pressure control, and anti-inflammatory responses. Studies in rat models have revealed its significance in conditions such as salt-sensitive hypertension, septic shock, and angiotensin II-induced renal injury, providing insights into potential therapeutic targets for these diseases.