Acute kidney injury has been a tough complex with increased mortality and morbidity. Inflammatory
responses, including innate and adaptive immune responses, involve in the initiation and
development of acute kidney injury, especially under the ischemic circumstances. Tubular cells and
distinct immune cell subgroups play a critical role in the pathogenesis of inflammation. Current gene
therapies show their benefits in renal repair. Here, we reviewed the renal inflammatory infiltration, inflammatory
mediators, oxidative stress and potential signaling pathways, which give rise to the kidney
diseases, in the mechanism of acute kidney injury. Recent studies showed diverse insights in understanding
the pathophysiological process of inflammation related renal injury and provided novel clinical
targets for ameliorating acute kidney injury by balancing the facilitation of repairing and prevention
of impairing. Interestingly, antisense oligonucleotides of target sequence, local electransfering on
solid organ and adenovirus-mediated certain gene overexpression have been promising strategies in
alleviating acute kidney injury.
Keywords: Acute kidney injury, Inflammation, Cytokines, Oxidative stress, Gene therapy, Dendritic cells.
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