Key result
Partial deficiency of mitochondrial SOD2, but not cytosolic SOD1, significantly impaired postischemic functional recovery in isolated mouse hearts (63% vs 92% in wild-type).
Why the study?
Does partial deficiency of SOD1 or SOD2 impair postischemic recovery of contractile function in isolated mouse hearts?
Does partial deficiency of SOD1 or SOD2 impair postischemic recovery of contractile function in isolated mouse hearts?
Absolute Event Rate: 63% vs 92%
Postischemic functional recovery is more sensitive to a partial deficiency of mitochondrial SOD2 than cytosolic SOD1, highlighting the critical role of mitochondrial SOD in tolerance to oxidative stress.
No takes yet. Share an insight, caveat, or question.
Mitochondrial SOD2 deficiency impairs postischemic recovery in mice; hypothesis-generating for compartment-specific antioxidant strategies in human ischemia-reperfusion.
Asimakis et al. (2002) studied Myocardial stunning. Heterozygous SOD1 (+/-) and SOD2 (+/-) knockout vs. Wild-type was evaluated on Recovery of heart rate multiplied by developed pressure (HR×DP) as a percentage of preischemic baseline. Partial deficiency of mitochondrial SOD2, but not cytosolic SOD1, significantly impaired postischemic functional recovery in isolated mouse hearts (63% vs 92% in wild-type).
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: