Defective Mitochondrial Fatty Acid Oxidation and Lipotoxicity in Kidney Diseases

Hee Seong Jang; Mi Ra Noh; Jinu Kim; Babu J. Padanilam

doi:10.3389/fmed.2020.00065

Defective Mitochondrial Fatty Acid Oxidation and Lipotoxicity in Kidney Diseases

Hee Seong Jang, Mi Ra Noh, Jinu Kim, Babu J. Padanilam

Research output: Contribution to journal › Review article › peer-review

Abstract

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 β-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.

Original language	English (US)
Article number	65
Journal	Frontiers in Medicine
Volume	7
DOIs	https://doi.org/10.3389/fmed.2020.00065
State	Published - Mar 12 2020
Externally published	Yes

Keywords

acute kidney injury
chronic kidney disease
diabetic nephropathy
fatty acid β-oxidation
glomerular nephropathy
lipotoxicity
mitochondria
polycystic kidney disease

ASJC Scopus subject areas

General Medicine

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10.3389/fmed.2020.00065

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title = "Defective Mitochondrial Fatty Acid Oxidation and Lipotoxicity in Kidney Diseases",

abstract = "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 β-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.",

keywords = "acute kidney injury, chronic kidney disease, diabetic nephropathy, fatty acid β-oxidation, glomerular nephropathy, lipotoxicity, mitochondria, polycystic kidney disease",

author = "Jang, {Hee Seong} and Noh, {Mi Ra} and Jinu Kim and Padanilam, {Babu J.}",

note = "Funding Information: This work was supported by NIH grants DK-116987, DK-120533, DK120846, and American Heart Association (AHA) Grant in Aid 15GRNT25080031 (BP), AHA postdoctoral fellowship Grant 15POST25130003 (H-SJ), and grants (NRF-2016R1C1B2012080 and NRF-2019R1F1A1041410) from the National Research Foundation of Korea (JK). Publisher Copyright: {\textcopyright} Copyright {\textcopyright} 2020 Jang, Noh, Kim and Padanilam.",

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doi = "10.3389/fmed.2020.00065",

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AU - Jang, Hee Seong

AU - Noh, Mi Ra

AU - Kim, Jinu

AU - Padanilam, Babu J.

N1 - Funding Information: This work was supported by NIH grants DK-116987, DK-120533, DK120846, and American Heart Association (AHA) Grant in Aid 15GRNT25080031 (BP), AHA postdoctoral fellowship Grant 15POST25130003 (H-SJ), and grants (NRF-2016R1C1B2012080 and NRF-2019R1F1A1041410) from the National Research Foundation of Korea (JK). Publisher Copyright: © Copyright © 2020 Jang, Noh, Kim and Padanilam.

PY - 2020/3/12

Y1 - 2020/3/12

N2 - 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 β-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.

AB - 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 β-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.

KW - acute kidney injury

KW - chronic kidney disease

KW - diabetic nephropathy

KW - fatty acid β-oxidation

KW - glomerular nephropathy

KW - lipotoxicity

KW - mitochondria

KW - polycystic kidney disease

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JO - Frontiers in Medicine

JF - Frontiers in Medicine

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ER -

Defective Mitochondrial Fatty Acid Oxidation and Lipotoxicity in Kidney Diseases

Abstract

Keywords

ASJC Scopus subject areas

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