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

123 Scopus citations

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

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

Access to Document

10.3389/fmed.2020.00065

Cite this

@article{6b61f0f210294f5ba60a4200e1245c8d,

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 = "Publisher Copyright: {\textcopyright} Copyright {\textcopyright} 2020 Jang, Noh, Kim and Padanilam.",

year = "2020",

month = mar,

day = "12",

doi = "10.3389/fmed.2020.00065",

language = "English (US)",

volume = "7",

journal = "Frontiers in Medicine",

issn = "2296-858X",

publisher = "Frontiers Media SA",

}

TY - JOUR

T1 - Defective Mitochondrial Fatty Acid Oxidation and Lipotoxicity in Kidney Diseases

AU - Jang, Hee Seong

AU - Noh, Mi Ra

AU - Kim, Jinu

AU - Padanilam, Babu J.

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

UR - http://www.scopus.com/inward/record.url?scp=85082663344&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85082663344&partnerID=8YFLogxK

U2 - 10.3389/fmed.2020.00065

DO - 10.3389/fmed.2020.00065

M3 - Review article

C2 - 32226789

AN - SCOPUS:85082663344

SN - 2296-858X

VL - 7

JO - Frontiers in Medicine

JF - Frontiers in Medicine

M1 - 65

ER -

Defective Mitochondrial Fatty Acid Oxidation and Lipotoxicity in Kidney Diseases

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this