肾
转录因子
急性肾损伤
β氧化
病理生理学
机制(生物学)
纤维化
化学
肾脏疾病
脂肪酸
医学
生物化学
生物
细胞生物学
内科学
内分泌学
基因
哲学
认识论
作者
Verónica Miguel,Santiago Lamas
标识
DOI:10.1016/j.kint.2021.09.018
摘要
The metabolic impairment of kidney tubular cells is a key mechanism underlying the pathophysiology of renal fibrosis. In particular, a drastic reduction in fatty acid oxidation is essentially responsible for the global energy failure occurring in the tubulointerstitial compartment. Piret et al. propose a novel transcriptional regulatory mechanism involving the decrease in the expression of Krüppel-like factor 15 in proximal tubular cells after kidney injury, which results in a major derangement of fatty acid oxidation.
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