title: Mitochondria in Acute Kidney Injury.
abstract: Acute kidney injury (AKI) continues to be a significant contributor to morbidity, mortality, and health care expenditure. In the United States alone, it is estimated that more than $10 billion is spent on AKI every year. Currently, there are no available therapies to treat established AKI. The mitochondrion is positioned to be a critical player in AKI with its dual role as the primary source of energy for each cell and as a key regulator of cell death. This review aims to cover the current state of research on the role of mitochondria in AKI, while also proposing potential therapeutic targets and future therapies.
authors.affiliation: Division of Nephrology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA.
authors.forename: Kenneth M
authors.initials: KM
authors.lastname: Ralto
authors.affiliation: Division of Nephrology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA. Electronic address: sparikh1@bidmc.harvard.edu.
authors.forename: Samir M
authors.initials: SM
authors.lastname: Parikh
mesh_terms: D058186:Acute Kidney Injury / Q000378:metabolism*; D006801:Humans; D008928:Mitochondria / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species
keywords: Mitochondria; acute kidney injury; metabolism; reactive oxygen species