Ischemia and reperfusion—from mechanism to translation

By H. Eltzschig, T. Eckle. Nature Medicine, 2011

3,229 citations recorded by the source corpus.

Ischemia and reperfusion–elicited tissue injury contributes to morbidity and mortality in a wide range of pathologies, including myocardial infarction, ischemic stroke, acute kidney injury, trauma, circulatory arrest, sickle cell disease and sleep apnea. Ischemia-reperfusion injury is also a major challenge during organ transplantation and cardiothoracic, vascular and general surgery. An imbalance in metabolic supply and demand within the ischemic organ results in profound tissue hypoxia and microvascular dysfunction. Subsequent reperfusion further enhances the activation of innate and adaptive immune responses and cell death programs. Recent advances in understanding the molecular and immunological consequences of ischemia and reperfusion may lead to innovative therapeutic strategies for treating patients with ischemia and reperfusion–associated tissue inflammation and organ dysfunction.

Subfields: Pathology and Forensic Medicine, Surgery

View Paper: https://www.semanticscholar.org/paper/d00c845265b5ba8b6193d5e8523ad08187b2258f

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In Pathology and Forensic Medicine

1. Nikolaos G. Frangogiannis
2. Sumanth D. Prabhu

In Surgery

1. Sumanth D. Prabhu
2. Nikolaos G. Frangogiannis

Citations in the corpus

• The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. (2016, background): “stranded RNA, single-stranded RNA, and complement, among others.(7,8,11,12,14) The PRRs are primarily the membrane-bound”
• Mesenchymal stromal cell-derived exosomes attenuate myocardial ischaemia-reperfusion injury through miR-182-regulated macrophage polarization (2019, background): “inflammatory reaction are intimately associated with myocardial injury and scar formation.(2,3) In this process, macrophages play an important role in the modulation of cardiac inflammation.”
• Reperfusion injury and reactive oxygen species: The evolution of a concept (2015, neutral): “injury, neonatal necrotizing enterocolitis) (Table 1) [1,49].”
• Mitochondrial dysfunction: mechanisms and advances in therapy (2024, background): “204,209 ROS contributes to cell and tissue impairment through lipid peroxidation within cell membranes and organelles, DNA oxidation, and the activation of matrix metalloproteinases and calpains.”
• A Unifying Mechanism for Mitochondrial Superoxide Production during Ischemia-Reperfusion Injury. (2016, background): “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).”