Myocardial ischemia-reperfusion injury: a neglected therapeutic target.
By D. Hausenloy, D. Yellon. Journal of Clinical Investigation, 2013
2,190 citations recorded by the source corpus.
Subfields: Biomedical Engineering, Cardiology and Cardiovascular Medicine, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/98c2600323332999c2865caa4d6e52cff2bfe0f3
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In Biomedical Engineering
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Citations in the corpus
- Mesenchymal stromal cell-derived exosomes attenuate myocardial ischaemia-reperfusion injury through miR-182-regulated macrophage polarization (2019, background): “Following myocardial I/R, a variety of damage-associated molecules are released from necrotic cardiac resident cells, thus induce an inflammatory cascade within the heart.(1) The initial pro-inflammatory response starts with clearance of dead cells and debris, and is gradually replaced by an anti-in”
- Ischemia/Reperfusion (2016, positive): “ventions confer protection against I/R injury by a mechanism that is dependent on p38 MAPK activation (328, 896).”
- A Unifying Mechanism for Mitochondrial Superoxide Production during Ischemia-Reperfusion Injury. (2016, background): “3 Introduction Ischemia-reperfusion (IR) injury occurs when the blood supply to a tissue is blocked for minutes to hours (ischemia), and then restored (reperfusion) (Eltzschig and Eckle, 2011; Hausenloy and Yellon, 2013).”
- Pathophysiology of Myocardial Infarction (2015, neutral): “…have suggested several promising therapeutic approaches and targets, including ischemic postcon-ditioning, inhibition of oxidative stress, attenuation of calcium overload, cyclosporine, correction of pH, suppression of proapoptotic pathways and activation of prosurvival pathways (92, 152, 197).”