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Prostaglandin E2 increases proximal tubule fluid reabsorption, and modulates cultured proximal tubule cell responses via EP1 and EP4 receptors.前列腺素E2可增加近端肾小管液体重吸收,并通过EP1和EP4受体调节培养的近端肾小管细胞反应。
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Magnesium and cardiovascular complications of chronic kidney disease.镁与慢性肾脏病的心血管并发症。
Nat Rev Nephrol. 2015 Jul;11(7):432-42. doi: 10.1038/nrneph.2015.74. Epub 2015 May 12.
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Diabetic neuropathic pain: Physiopathology and treatment.糖尿病性神经病理性疼痛:生理病理学与治疗
World J Diabetes. 2015 Apr 15;6(3):432-44. doi: 10.4239/wjd.v6.i3.432.
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Gut dysbiosis is linked to hypertension.肠道微生物群失调与高血压有关。
Hypertension. 2015 Jun;65(6):1331-40. doi: 10.1161/HYPERTENSIONAHA.115.05315. Epub 2015 Apr 13.
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Management of diabetic nephropathy: Recent progress and future perspective.糖尿病肾病的管理:近期进展与未来展望
Diabetes Metab Syndr. 2015 Oct-Dec;9(4):343-58. doi: 10.1016/j.dsx.2015.02.008. Epub 2015 Mar 6.
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Role of COX-2/mPGES-1/prostaglandin E2 cascade in kidney injury.COX-2/mPGES-1/前列腺素E2级联反应在肾损伤中的作用。
Mediators Inflamm. 2015;2015:147894. doi: 10.1155/2015/147894. Epub 2015 Feb 1.
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EP3 receptor deficiency attenuates pulmonary hypertension through suppression of Rho/TGF-β1 signaling.EP3受体缺陷通过抑制Rho/TGF-β1信号传导减轻肺动脉高压。
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Leptin and insulin act on POMC neurons to promote the browning of white fat.瘦素和胰岛素作用于促黑素细胞激素神经元,以促进白色脂肪的褐色化。
Cell. 2015 Jan 15;160(1-2):88-104. doi: 10.1016/j.cell.2014.12.022.
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Obesity bias, medical technology, and the hormonal hypothesis: should we stop demonizing fat people?肥胖偏见、医疗技术和激素假说:我们是否应该停止妖魔化胖人?
Am J Med. 2015 May;128(5):456-60. doi: 10.1016/j.amjmed.2014.11.024. Epub 2014 Dec 20.
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Activation of prostaglandin E2-EP4 signaling reduces chemokine production in adipose tissue.前列腺素E2-EP4信号通路的激活可减少脂肪组织中趋化因子的产生。
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前列腺素E2、肾脏疾病与心血管风险:超越高血压和糖尿病

PGE2, Kidney Disease, and Cardiovascular Risk: Beyond Hypertension and Diabetes.

作者信息

Nasrallah Rania, Hassouneh Ramzi, Hébert Richard L

机构信息

Department of Cellular and Molecular Medicine, Kidney Research Centre, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada.

Department of Cellular and Molecular Medicine, Kidney Research Centre, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada

出版信息

J Am Soc Nephrol. 2016 Mar;27(3):666-76. doi: 10.1681/ASN.2015050528. Epub 2015 Aug 28.

DOI:10.1681/ASN.2015050528
PMID:26319242
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4769209/
Abstract

An important measure of cardiovascular health is obtained by evaluating the global cardiovascular risk, which comprises a number of factors, including hypertension and type 2 diabetes, the leading causes of illness and death in the world, as well as the metabolic syndrome. Altered immunity, inflammation, and oxidative stress underlie many of the changes associated with cardiovascular disease, diabetes, and the metabolic syndrome, and recent efforts have begun to elucidate the contribution of PGE2 in these events. This review summarizes the role of PGE2 in kidney disease outcomes that accelerate cardiovascular disease, highlights the role of cyclooxygenase-2/microsomal PGE synthase 1/PGE2 signaling in hypertension and diabetes, and outlines the contribution of PGE2 to other aspects of the metabolic syndrome, particularly abdominal adiposity, dyslipidemia, and atherogenesis. A clearer understanding of the role of PGE2 could lead to new avenues to improve therapeutic options and disease management strategies.

摘要

评估全球心血管风险是衡量心血管健康的一项重要指标,全球心血管风险包含多个因素,包括高血压和2型糖尿病(全球疾病和死亡的主要原因)以及代谢综合征。免疫、炎症和氧化应激的改变是许多与心血管疾病、糖尿病和代谢综合征相关变化的基础,最近的研究已开始阐明前列腺素E2(PGE2)在这些事件中的作用。本综述总结了PGE2在加速心血管疾病的肾脏疾病结局中的作用,强调了环氧化酶-2/微粒体PGE合酶1/PGE2信号通路在高血压和糖尿病中的作用,并概述了PGE2对代谢综合征其他方面的影响,特别是腹部肥胖、血脂异常和动脉粥样硬化的形成。更清楚地了解PGE2的作用可能会带来改善治疗选择和疾病管理策略的新途径。