Mitochondrial Metabolism in Acute Kidney Injury

Amanda J. Clark, Samir M. Parikh

Research output: Contribution to journalReview articlepeer-review

21 Scopus citations

Abstract

Summary: The kidney is a highly metabolic organ that requires substantial adenosine triphosphate for the active transport required to maintain water and solute reabsorption. Aberrations in energy availability and energy utilization can lead to cellular dysfunction and death. Mitochondria are essential for efficient energy production. The pathogenesis of acute kidney injury is complex and varies with different types of injury. However, multiple distinct acute kidney injury syndromes share a common dysregulation of energy metabolism. Pathways of energy metabolism and mitochondrial dysfunction are emerging as critical drivers of acute kidney injury and represent new potential targets for treatment. This review shows the basic metabolic pathways that all cells depend on for life; describes how the kidney optimizes those pathways to meet its anatomic, physiologic, and metabolic needs; summarizes the importance of metabolic and mitochondrial dysfunction in acute kidney injury; and analyzes the mitochondrial processes that become dysregulated in acute kidney injury including mitochondrial dynamics, mitophagy, mitochondrial biogenesis, and changes in mitochondrial energy metabolism.

Original languageEnglish (US)
Pages (from-to)101-113
Number of pages13
JournalSeminars in nephrology
Volume40
Issue number2
DOIs
StatePublished - Mar 2020
Externally publishedYes

Keywords

  • Acute kidney injury
  • metabolism
  • mitochondria

ASJC Scopus subject areas

  • Nephrology

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