Abstract
Ischemia-reperfusion injury (IRI) is common to several pathologic conditions, including myocardial infarction, stroke, acute kidney injury, and delayed graft function after kidney transplantation.1 Clearance of apoptotic and necrotic cells by resident immune or epithelial cellsS1,S2 prevents release of harmful intracellular proinflammatory mediators, and is thought to represent an important mechanism to dampen secondary tissue damage and promote repair after acute injury, including IRI.2,3,S3,S4 In the kidney, proximal tubular epithelial cells (PTECs) are highly susceptible to apoptosis and necrosis after IRI.
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