Cardiac-specific deletion of GCN5L1 restricts recovery from ischemia-reperfusion injury
Janet R. Manning(University of Pittsburgh), Iain Scott(Beijing Institute of Technology), Dharendra Thapa(West Virginia University), Catherine Corey, Michael N. Sack(National Institutes of Health), Michael W. Stoner(University of Pittsburgh), Sruti Shiva(University of Pittsburgh), Manling Zhang(Kunming University of Science and Technology), Charles F. McTiernan(University of Pittsburgh), Javier Traba(National Institutes of Health)
Cited by 63
Related Papers
Mitochondrial reactive oxygen species promote production of proinflammatory cytokines and are elevated in TNFR1-associated periodic syndrome (TRAPS)
|The Journal of Experimental Medicine|2011|854
Fatty Acid Oxidation Enzyme Gene Expression Is Downregulated in the Failing Heart
|Circulation|1996|681
PINK1 deficiency impairs mitochondrial homeostasis and promotes lung fibrosis
|Journal of Clinical Investigation|2014|613
Nitrite augments tolerance to ischemia/reperfusion injury via the modulation of mitochondrial electron transfer
|The Journal of Experimental Medicine|2007|561