TY - JOUR
T1 - SOD2 and the Mitochondrial UPR
T2 - Partners Regulating Cellular Phenotypic Transitions
AU - He, Chenxia
AU - Hart, Peter C.
AU - Germain, Doris
AU - Bonini, Marcelo G.
N1 - Funding Information:
The authors acknowledge the following agencies for providing funds that support research in their laboratories; the US Department of Defense (grant W911NF-15-1-0410 to M.G.B.); the National Heart, Lung, and Blood Institute [grant 2RO1HL125356 to M.G.B. (MPI)], and the National Cancer Institute (grant 1RO1CA172046-01A1 to D.G.).
Publisher Copyright:
© 2016 Elsevier Ltd
PY - 2016/7/1
Y1 - 2016/7/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84970028289&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84970028289&partnerID=8YFLogxK
U2 - 10.1016/j.tibs.2016.04.004
DO - 10.1016/j.tibs.2016.04.004
M3 - Review article
C2 - 27180143
AN - SCOPUS:84970028289
SN - 0968-0004
VL - 41
SP - 568
EP - 577
JO - Trends in Biochemical Sciences
JF - Trends in Biochemical Sciences
IS - 7
ER -