title: Mitochondrial Homeostasis in Acute Organ Failure.
abstract: The kidneys compose approximately 0.5% of the body mass but consume about 10% of the oxygen in cellular respiration. This discordance is due to the high energy demands on the kidney for reabsorption of filtered blood components and makes the kidney sensitive to mitochondrial stress, the primary source of cellular ATP. Regardless of the etiology, acute kidney injury (AKI) almost always involves aspects of mitochondrial dysfunction. Recent evidence from experimental models suggests that preserving mitochondrial function or promoting mitochondrial repair rescues renal function during AKI. In this review we discuss the effect of AKI on disruption of mitochondrial homeostasis, and how the dynamic processes of mitochondrial biogenesis, fission/fusion, and mitophagy influence renal injury and recovery.
authors.affiliation: Center for Cell Death, Injury, and Regeneration, Department of Drug Discovery and Biomedical Sciences, Medical University of South Carolina, 280 Calhoun Street, Charleston, South Carolina 29425.
authors.forename: L Jay
authors.initials: LJ
authors.lastname: Stallons
authors.affiliation: Division of Nephrology, Department of Medicine, Medical University of South Carolina, 70 President Street, Charleston, SC 29425.
authors.forename: Jason A
authors.initials: JA
authors.lastname: Funk
authors.affiliation: Center for Cell Death, Injury, and Regeneration, Department of Drug Discovery and Biomedical Sciences, Medical University of South Carolina, 280 Calhoun Street, Charleston, South Carolina 29425 ; Ralph H. Johnson Veterans Affairs Medical Center, 109 Bee Street, Charleston, South Carolina 29401.
authors.forename: Rick G
authors.initials: RG
authors.lastname: Schnellmann
keywords: Acute kidney injury; Autophagy; Biogenesis; Dynamics; Ischemia/reperfusion; Kidney; Mitochondria; Mitophagy; PGC-1α; Pathobiology; Sepsis