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多组学揭示的肾脏代偿性肥大中的信号机制。

Signaling mechanisms in renal compensatory hypertrophy revealed by multi-omics.

机构信息

Epithelial Systems Biology Laboratory, Systems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.

Division of Nephrology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

出版信息

Nat Commun. 2023 Jun 16;14(1):3481. doi: 10.1038/s41467-023-38958-9.

Abstract

Loss of a kidney results in compensatory growth of the remaining kidney, a phenomenon of considerable clinical importance. However, the mechanisms involved are largely unknown. Here, we use a multi-omic approach in a unilateral nephrectomy model in male mice to identify signaling processes associated with renal compensatory hypertrophy, demonstrating that the lipid-activated transcription factor peroxisome proliferator-activated receptor alpha (PPARα) is an important determinant of proximal tubule cell size and is a likely mediator of compensatory proximal tubule hypertrophy.

摘要

肾脏的丧失会导致剩余肾脏的代偿性生长,这是一个具有重要临床意义的现象。然而,涉及的机制在很大程度上是未知的。在这里,我们在雄性小鼠的单侧肾切除术模型中使用多组学方法来鉴定与肾代偿性肥大相关的信号过程,证明脂激活转录因子过氧化物酶体增殖物激活受体α(PPARα)是近端小管细胞大小的重要决定因素,并且可能是代偿性近端小管肥大的介质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b74b/10276015/01c087e02da5/41467_2023_38958_Fig1_HTML.jpg

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