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肾脏中的环氧化酶-2:有益、有害,还是两者皆有?

Cyclooxygenase-2 in the kidney: good, BAD, or both?

机构信息

Renal Division, Department of Medicine, Emory University, Atlanta, Georgia, USA.

Renal Division, Department of Medicine, Emory University, Atlanta, Georgia, USA.

出版信息

Kidney Int. 2011 Nov;80(9):905-907. doi: 10.1038/ki.2011.263.

Abstract

Hypertonic stress in the kidney inner medulla is common, yet inner medullary cells adapt to limit cell death. Küper et al. have identified a cell-survival response by which increased cyclooxygenase-2 (COX-2) stimulates a prostaglandin E(2) (PGE(2))/protein kinase A (PKA)-mediated inactivation of the pro-apoptotic protein BAD. However, the PGE(2)/PKA pathway is not the only means to inactivate BAD and limit cell death. This Commentary shows a broader picture of this pathway to examine the kidney's BAD options.

摘要

肾脏髓质中的高渗应激很常见,但髓质细胞会适应以限制细胞死亡。Küper 等人发现了一种细胞存活反应,其中增加的环氧化酶-2(COX-2)刺激前列腺素 E(PGE(2))/蛋白激酶 A(PKA)介导的促凋亡蛋白 BAD 的失活。然而,PGE(2)/PKA 途径并不是使 BAD 失活和限制细胞死亡的唯一途径。本评论展示了该途径的更广泛图景,以检查肾脏的 BAD 选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edc9/3664549/1c35b6fe57bb/nihms460444f1.jpg

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