Signaling mechanisms in renal compensatory hypertrophy revealed by multi-omics

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作者
Hiroaki Kikuchi
Chung-Lin Chou
Chin-Rang Yang
Lihe Chen
Hyun Jun Jung
Euijung Park
Kavee Limbutara
Benjamin Carter
Zhi-Hong Yang
Julia F. Kun
Alan T. Remaley
Mark A. Knepper
机构
[1] National Institutes of Health,Epithelial Systems Biology Laboratory, Systems Biology Center, National Heart, Lung, and Blood Institute
[2] Johns Hopkins University School of Medicine,Division of Nephrology, Department of Medicine
[3] Chulalongkorn University,The Center of Excellence in Systems Biology, Faculty of Medicine
[4] Lung and Blood Institute,Laboratory of Epigenome Biology, Systems Biology Center, National Heart
[5] NIH,Lipoprotein Metabolism Section, Translational Vascular Medicine Branch, National Heart, Lung and Blood Institute
[6] National Institutes of Health,undefined
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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.
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