New directions for protecting the heart against ischaemia-reperfusion injury: targeting the Reperfusion Injury Salvage Kinase (RISK)-pathway.

By D. Hausenloy, D. Yellon. Cardiovascular Research, 2004

1,088 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/2fac2ac9523de9362133a70e77407811fa2d8bcf

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cardiology and Cardiovascular Medicine

1. E. Murphy
2. C. Steenbergen
3. M. Mocanu
4. D. Yellon
5. A. Tsang
6. D. Hausenloy
7. G. Heusch

In Molecular Biology

1. E. Murphy
2. C. Steenbergen
3. M. Mocanu
4. A. Tsang
5. D. Yellon
6. D. Hausenloy
7. S. Lim
8. R. C. Lai

In Pathology and Forensic Medicine

1. E. Murphy
2. C. Steenbergen
3. M. Mocanu
4. D. Yellon
5. D. Hausenloy
6. A. Tsang
7. G. Heusch
8. S. Cadenas

Citations in the corpus

• Postconditioning: A Form of “Modified Reperfusion” Protects the Myocardium by Activating the Phosphatidylinositol 3-Kinase–Akt Pathway (2004, methodology): “02% dimethyl sulfoxide (DMSO) vehicle (n 4) for the first 15 minutes of reperfusion; (2) IPC (n 11), comprising 2 cycles of 5 minutes of global ischemia followed by 10 minutes of reperfusion before the index ischemia; (3) Postcond (n 10), comprising 6 cycles of 10 seconds of reperfusion followed by ”
• Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. (2008, methodology): “The RISK pathway was originally used to describe activation of survival kinases by addition of agonists such as adenosine and insulin at the start of reperfusion (102).”
• Reduction of myocardial infarct size by human mesenchymal stem cell conditioned medium. (2008, background): “Reperfusion injury causes cell death through apoptosis rather than necrosis (Dumont et al., 2001; Eefting et al., 2004; Hausenloy and Yellon, 2004).”
• 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, background): “Finally, we also predicted that the presence of enzymatically active CD73 on exosomes would produce adenosine from extracellular ATP to activate RISK and enhance myocardial viability (Hausenloy and Yellon, 2004).”
• Glucagon-like peptide 1 can directly protect the heart against ischemia/reperfusion injury. (2005, methodology): “This kinase has been clearly associated with myocardial protection in the setting of ischemic/reperfusion injury (13) as well as myocardial preconditioning (14,15).”