SOD2 and the Mitochondrial UPR: Partners Regulating Cellular Phenotypic Transitions

Chenxia He, Peter C. Hart, Doris Germain, Marcelo G. Bonini*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

29 Scopus citations


ATP and reactive oxygen species (ROS) are signaling molecules that control cellular function and phenotype. Mitochondria produce both ATP and ROS. Since the electrons needed to generate either ATP or ROS originate from NADH/FADH2, the mechanism through which electrons flow towards oxygen determines yields and whether ATP or ROS prevails. Alterations in the electron flow impact cells dramatically, such as by supporting specialization (which requires high ATP) or imposing dedifferentiation. High ROS, facilitated by enzymes such as superoxide dismutase 2 (SOD2) that enhance mitochondrial hydrogen peroxide (mtH2O2), are normally linked to dedifferentiation of somatic cells. Here we propose that combined high mtH2O2 and mitochondrial unfolded protein response (UPRmt) activation are essential for somatic dedifferentiation programs and the acquisition of stem-like properties in reparative processes and disease.

Original languageEnglish (US)
Pages (from-to)568-577
Number of pages10
JournalTrends in Biochemical Sciences
Issue number7
StatePublished - Jul 1 2016
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology


Dive into the research topics of 'SOD2 and the Mitochondrial UPR: Partners Regulating Cellular Phenotypic Transitions'. Together they form a unique fingerprint.

Cite this