Mitochondria in Acute Kidney Injury

Kenneth M Ralto; Samir M Parikh

doi:10.1016/j.semnephrol.2016.01.005

Mitochondria in Acute Kidney Injury

Semin Nephrol. 2016 Jan;36(1):8-16. doi: 10.1016/j.semnephrol.2016.01.005.

Authors

Kenneth M Ralto¹, Samir M Parikh²

Affiliations

¹ Division of Nephrology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA.
² Division of Nephrology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA. Electronic address: sparikh1@bidmc.harvard.edu.

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.

Keywords: Mitochondria; acute kidney injury; metabolism; reactive oxygen species.

Publication types

Research Support, N.I.H., Extramural
Review

MeSH terms

Acute Kidney Injury / metabolism*
Humans
Mitochondria / physiology*
Reactive Oxygen Species / metabolism

Substances

Reactive Oxygen Species

Abstract

Publication types

MeSH terms

Substances

Grants and funding