ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Myristoylated methionine sulfoxide reductase A protects the heart from ischemia-reperfusion injury.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- Protein lipidation in cardiovascular homeostasis, development, and disease.Clinical science (London, England : 1979) · 2026Review
- Processes and therapeutic perspectives of acylation modifications of lysine and cysteine in tumors.Cell communication and signaling : CCS · 2026Review
- Post-translational acylation of proteins in cardiac hypertrophy.Nature reviews. Cardiology · 2025Review
- Association between antioxidant metabolites and N-terminal fragment brain natriuretic peptides in insulin-resistant individuals.Cardiovascular endocrinology & metabolism · 2024Article
- Genes and Longevity of Lifespan.International journal of molecular sciences · 2022Review
- Mitochondrial redox regulation and myocardial ischemia-reperfusion injury.American journal of physiology. Cell physiology · 2022Review
- Mitochondrial-targeted methionine sulfoxide reductase overexpression increases the production of oxidative stress in mitochondria from skeletal muscle.Aging pathobiology and therapeutics · 2020Article
- Loss of methionine sulfoxide reductases increases resistance to oxidative stress.Free radical biology & medicine · 2019Article
- Effects of Post-translational Modifications on Membrane Localization and Signaling of Prostanoid GPCR-G Protein Complexes and the Role of Hypoxia.The Journal of membrane biology · 2019Review
- Methionine in Proteins: It's Not Just for Protein Initiation Anymore.Neurochemical research · 2019Review
- The Oxidized Protein Repair Enzymes Methionine Sulfoxide Reductases and Their Roles in Protecting against Oxidative Stress, in Ageing and in Regulating Protein Function.Antioxidants (Basel, Switzerland) · 2018Review
- Myristoylated methionine sulfoxide reductase A is a late endosomal protein.The Journal of biological chemistry · 2018Article
- Redox homeostasis and age-related deficits in neuromuscular integrity and function.Journal of cachexia, sarcopenia and muscle · 2017Review
- Article
- Methionine sulfoxide reductase B1 deficiency does not increase high-fat diet-induced insulin resistance in mice.Free radical research · 2017Article
- Effects of transgenic methionine sulfoxide reductase A (MsrA) expression on lifespan and age-dependent changes in metabolic function in mice.Redox biology · 2016Article
- A Methionine Residue Promotes Hyperoxidation of the Catalytic Cysteine of Mouse Methionine Sulfoxide Reductase A.Biochemistry · 2016Article
- Deletion of Methionine Sulfoxide Reductase A Does Not Affect Atherothrombosis but Promotes Neointimal Hyperplasia and Extracellular Signal-Regulated Kinase 1/2 Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Review
- MsrA Overexpression Targeted to the Mitochondria, but Not Cytosol, Preserves Insulin Sensitivity in Diet-Induced Obese Mice.PloS one · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Methionine sulfoxide reductase A (MsrA) catalytically scavenges reactive oxygen species and also repairs oxidized methionines in proteins. Increasing MsrA protects cells and organs from a variety of oxidative stresses while decreasing MsrA enhances damage, but the mechanisms of action have not been elucidated. A single gene encodes MsrA of which ∼25% is targeted to the mitochondria, a major site of reactive oxygen species production. The other ∼75% is targeted to the cytosol and is posttranslationally modified by myristoylation. To determine the relative importance of MsrA in each compartment in protecting against ischemia-reperfusion damage, we created a series of transgenic mice overexpressing MsrA targeted to the mitochondria or the cytosol. We used a Langendorff model of ischemia-reperfusion and assayed both the rate pressure product and infarct size following ischemia and reperfusion as measures of injury. While the mitochondrially targeted MsrA was expected to be protective, it was not. Notably, the cytosolic form was protective but only if myristoylated. The nonmyristoylated, cytosolic form offered no protection against injury. We conclude that cytosolic MsrA protects the heart from ischemia-reperfusion damage. The requirement for myristoylation suggests that MsrA must interact with a hydrophobic domain to provide protection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.