Regulation of ENaC-Mediated Sodium Reabsorption by Peroxisome Proliferator-Activated Receptors.
Regulation of ENaC-Mediated Sodium Reabsorption by Peroxisome Proliferator-Activated Receptors.
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DOI：
10.1155/2010/703735
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发表时间：
2010
期刊：
影响因子：
2.9
通讯作者：
Staruschenko A
中科院分区：
文献类型：
--
作者：
Pavlov TS;Imig JD;Staruschenko A
过氧化物酶体增殖激活受体（PPARs）是类固醇激素受体超家族的成员，响应脂质和葡萄糖稳态的变化。过氧化物酶体增殖物激活受体亚型γ (PPARγ)作为抗糖尿病药物的靶点，以及它在响应内源性化合物如前列腺素J2中的作用受到了广泛的关注。然而，噻唑烷二酮（TZDs）， PPARγ的合成激动剂与液体潴留和水肿密切相关，作为潜在的严重副作用。上皮性钠通道（ENaC）代表了肾集管钠吸收的限速步骤。因此，ENaC是影响全身血容量和血压的中枢效应物。PPARγ激动剂对ENaC活性的作用仍有争议。虽然PPARγ激动剂被证明可以刺激ENaC介导的肾盐吸收，可能是通过血清和糖皮质激素调节激酶1 (SGK1)，但其他研究报道PPARγ激动剂诱导的液体潴存与ENaC活性无关。本论文对ENaC和ENaC介导的钠转运以及ppar，特别是PPARγ介导的其他几种上皮通道/转运体的控制和功能提供了新的见解。花生四烯酸（AA）代谢物在ppar依赖机制中的潜在贡献也进行了讨论。
Peroxisome proliferator-activated receptors (PPARs) are members of a steroid hormone receptor superfamily that responds to changes in lipid and glucose homeostasis. Peroxisomal proliferator-activated receptor subtype γ (PPARγ) has received much attention as the target for antidiabetic drugs, as well as its role in responding to endogenous compounds such as prostaglandin J2. However, thiazolidinediones (TZDs), the synthetic agonists of the PPARγ are tightly associated with fluid retention and edema, as potentially serious side effects. The epithelial sodium channel (ENaC) represents the rate limiting step for sodium absorption in the renal collecting duct. Consequently, ENaC is a central effector impacting systemic blood volume and pressure. The role of PPARγ agonists on ENaC activity remains controversial. While PPARγ agonists were shown to stimulate ENaC-mediated renal salt absorption, probably via Serum- and Glucocorticoid-Regulated Kinase 1 (SGK1), other studies reported that PPARγ agonist-induced fluid retention is independent of ENaC activity. The current paper provides new insights into the control and function of ENaC and ENaC-mediated sodium transport as well as several other epithelial channels/transporters by PPARs and particularly PPARγ. The potential contribution of arachidonic acid (AA) metabolites in PPAR-dependent mechanisms is also discussed.
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DOI：
10.1073/pnas.96.5.2514
发表时间：
1999-03-02
影响因子：
11.1
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DOI：
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影响因子：
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作者：
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