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Extracellular vesicles for treatment of solid organ ischemia–reperfusion injury
Author(s) -
Ali Mojahid,
Pham Anthony,
Wang Xinghua,
Wolfram Joy,
Pham Si
Publication year - 2020
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/ajt.16164
Subject(s) - medicine , ischemia , reperfusion injury , inflammation , extracellular vesicle , hypoxia (environmental) , stroke (engine) , pharmacology , bioinformatics , microvesicles , immunology , biology , microrna , mechanical engineering , biochemistry , chemistry , organic chemistry , oxygen , engineering , gene
As the incidence of ischemia–reperfusion (I‐R) injury has substantially increased, there is a pressing need to develop effective strategies to treat this global health issue. I‐R injury can affect all organs and is associated with high morbidity and mortality rates. Pathological settings such as myocardial infarction, stroke, hemorrhagic shock, and solid organ transplant are particularly prone to cause I‐R injury. Ischemia (hypoxia) and/or reperfusion (reoxygenation) induces various forms of cellular and structural damage. A major cause of damage is local inflammatory responses, which may spread to produce more advanced systemic inflammation. Management of I‐R injury relies primarily on supportive measures, as specific treatment strategies are lacking. Extracellular vesicles (EVs) are cell‐secreted nano‐scale structures containing various biomolecules involved in cell communication and multiple physiological processes. EVs derived from certain cell types have been shown to exhibit anti‐inflammatory, antioxidant, and angiogenic properties. This review provides an overview of EV‐based therapeutics for I‐R injury in kidneys, liver, heart, lungs, and brain. Additionally, the mechanisms by which EVs protect against I‐R injury are discussed. Promising preclinical findings highlight the potential clinical use of EVs for I‐R injury.