代偿性肥大
近曲小管
肌肉肥大
肾
转录因子
肾肥大
过氧化物酶体增殖物激活受体
肾切除术
肾小管
内科学
生物
内分泌学
受体
小管
调解人
医学
生物信息学
基因
生物化学
糖尿病肾病
作者
Hiroaki Kikuchi,Chung‐Lin Chou,Chin‐Rang Yang,Lihe Chen,Hyun Jun Jung,Euijung Park,Kavee Limbutara,Benjamin C. Carter,Yang Zhihong,Juergen F. J. Kun,Alan T. Remaley,Mark A. Knepper
标识
DOI:10.1038/s41467-023-38958-9
摘要
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.
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