Acidosis overrides oxygen deprivation to maintain mitochondrial function and cell survival

  • Khacho M
  • Tarabay M
  • Patten D
 et al. 
  • 113


    Mendeley users who have this article in their library.
  • 33


    Citations of this article.


Sustained cellular function and viability of high-energy demanding post-mitotic cells rely on the continuous supply of ATP. The utilization of mitochondrial oxidative phosphorylation for efficient ATP generation is a function of oxygen levels. As such, oxygen deprivation, in physiological or pathological settings, has profound effects on cell metabolism and survival. Here we show that mild extracellular acidosis, a physiological consequence of anaerobic metabolism, can reprogramme the mitochondrial metabolic pathway to preserve efficient ATP production regardless of oxygen levels. Acidosis initiates a rapid and reversible homeostatic programme that restructures mitochondria, by regulating mitochondrial dynamics and cristae architecture, to reconfigure mitochondrial efficiency, maintain mitochondrial function and cell survival. Preventing mitochondrial remodelling results in mitochondrial dysfunction, fragmentation and cell death. Our findings challenge the notion that oxygen availability is a key limiting factor in oxidative metabolism and brings forth the concept that mitochondrial morphology can dictate the bioenergetic status of post-mitotic cells.

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document


  • Mireille Khacho

  • Michelle Tarabay

  • David Patten

  • Pamela Khacho

  • Jason G. MacLaurin

  • Jennifer Guadagno

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free