In mice ventilated for 6 h, SS31 treatment prevented mitochondrial ROS production.
In plain wordsIn ventilated mice, SS31 prevented the rise in mitochondrial reactive oxygen species.
- Peptide
- Elamipretide (SS-31)
- Outcome
- DecreaseMitochondrial ROS production during 6 h ventilation
- Study
mousen: not reported in source
Mechanically ventilated mouse diaphragm (6 h and 12 h)- Comparator
- Mechanical ventilation without SS31
- Outcome group
- Mitochondrial function · Respiratory
- Studied dose
- Dose not stated
Source sentences
Preventing mROS production by SS31 treatment does not affect the TGFβ1 and STAT3 activation, which suggests that mitochondrial oxidative stress is a downstream pathway to TGFβ1 and STAT3, early involved in VIDD.
2 context sentences(design, population, supporting numbers)
6 h of mechanical ventilation (MV) resulted in increased mitochondrial ROS production, reduction of mitochondrial aconitase activity, increased oxidation, S-nitrosylation, S-glutathionylation and Ser-2844 phosphorylation of RyR1, depletion of stabilizing subunit calstabin1 from RyR1, increased SR Ca2+ leak.
In mice diaphragms mechanically ventilated for short (6 h) and long (12 h) period