Defective Mitochondrial Fatty Acid Oxidation and Lipotoxicity in Kidney Diseases

被引：130

作者：

Jang, Hee-Seong ^{[1
]}

Noh, Mi Ra ^{[1
]}

Kim, Jinu ^{[1
,2
,3
]}

Padanilam, Babu J. ^{[1
,4
]}

机构：

[1] Univ Nebraska, Med Ctr, Dept Cellular & Integrat Physiol, Omaha, NE 68182 USA

[2] Jeju Natl Univ, Sch Med, Dept Anat, Jeju, South Korea

[3] Jeju Natl Univ, Interdisciplinary Grad Program Adv Convergence Te, Jeju, South Korea

[4] Univ Nebraska, Med Ctr, Sect Nephrol, Internal Med, Omaha, NE 68182 USA

来源：

FRONTIERS IN MEDICINE | 2020年 / 7卷

基金：

新加坡国家研究基金会;

关键词：

mitochondria; fatty acid beta-oxidation; lipotoxicity; acute kidney injury; chronic kidney disease; diabetic nephropathy; polycystic kidney disease; glomerular nephropathy; PPAR-ALPHA AGONIST; NF-KAPPA-B; POLYCYSTIC KIDNEY; BETA-OXIDATION; LIPID NEPHROTOXICITY; ENERGY-METABOLISM; PROXIMAL TUBULES; FENOFIBRATE; ACCUMULATION; PROTECTS;

D O I：

10.3389/fmed.2020.00065

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The kidney is a highly metabolic organ and uses high levels of ATP to maintain electrolyte and acid-base homeostasis and reabsorb nutrients. Energy depletion is a critical factor in development and progression of various kidney diseases including acute kidney injury (AKI), chronic kidney disease (CKD), and diabetic and glomerular nephropathy. Mitochondrial fatty acid beta-oxidation (FAO) serves as the preferred source of ATP in the kidney and its dysfunction results in ATP depletion and lipotoxicity to elicit tubular injury and inflammation and subsequent fibrosis progression. This review explores the current state of knowledge on the role of mitochondrial FAO dysfunction in the pathophysiology of kidney diseases including AKI and CKD and prospective views on developing therapeutic interventions based on mitochondrial energy metabolism.

引用

页数：8

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