Oxidative stress and autophagy: Crucial modulators of kidney injury Review uri icon

Overview

MeSH Major

  • Acute Kidney Injury
  • Autophagy
  • Kidney
  • Oxidative Stress
  • Reactive Oxygen Species
  • Renal Insufficiency, Chronic

abstract

  • Both acute kidney injury (AKI) and chronic kidney disease (CKD) that lead to diminished kidney function are interdependent risk factors for increased mortality. If untreated over time, end stage renal disease (ESRD) is an inevitable outcome. Acute and chronic kidney diseases occur partly due to imbalance between the molecular mechanisms that govern oxidative stress, inflammation, autophagy and cell death. Oxidative stress refers to the cumulative effects of highly reactive oxidizing molecules that cause cellular damage. Autophagy removes damaged organelles, protein aggregates and pathogens by recruiting these substrates into double membrane vesicles called autophagosomes which subsequently fuse with lysosomes. Mounting evidence suggests that both oxidative stress and autophagy are significantly involved in kidney health and disease. However, very little is known about the signaling processes that link them. This review is focused on understanding the role of oxidative stress and autophagy in kidney diseases. In this review, we also discuss the potential relationships between oxidative stress and autophagy that may enable the development of better therapeutic intervention to halt the progression of kidney disease and promote its repair and resolution.

publication date

  • April 2015

Research

keywords

  • Review

Identity

Language

  • eng

PubMed Central ID

  • PMC4803795

Digital Object Identifier (DOI)

  • 10.1016/j.redox.2015.01.001

PubMed ID

  • 25613291

Additional Document Info

start page

  • 208

end page

  • 14

volume

  • 4