Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury.

By E. Murphy, C. Steenbergen. Physiological Reviews, 2008

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Mitochondrial dysfunction: mechanisms and advances in therapy (2024, background): “388 Xenogeneic mitochondria, while presenting an abundant and diverse reservoir, are currently con ﬁ ned to the experimental realm, predominantly due to heightened immunogenic risks and profound ethical considerations.”
Mesenchymal stem cell-derived exosomes increase ATP levels, decrease oxidative stress and activate PI3K/Akt pathway to enhance myocardial viability and prevent adverse remodeling after myocardial ischemia/reperfusion injury. (2013, neutral): “Exosome treatment restores energy depletion and redox state within 30 min after I/R Mitochondrial dysfunction is one of the most important determinants of viability loss after I/R injury (Murphy and Steenbergen, 2008).”
The importance of antioxidants which play the role in cellular response against oxidative/nitrosative stress: current state (2015, background): “However, there is a constant leak of a few electrons into the mitochondrial matrix and this results in the formation of superoxide [4, 5].”
A Unifying Mechanism for Mitochondrial Superoxide Production during Ischemia-Reperfusion Injury. (2016, result): “This view is consistent with the bewildering range of interventions that decrease IR injury (Burwell et al., 2009; Kornfeld et al., 2015; Murphy et al., 2012; Murphy and Steenbergen, 2008a, b).”