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Abstract
Contrast-induced acute kidney injury (CI-AKI) is the third common cause of acute kidney injury (AKI), which is associated with poor short- and long-term outcomes. Currently, effective therapy strategy for CI-AKI remains lacking. Stanniocalcin-1 (STC1) is a conserved glycoprotein with antiapoptosis and anti-inflammatory functions, but the role of STC1 in controlling CI-AKI is unknown. Here, we demonstrated a protective role of STC1 in contrast-induced injury in cultured renal tubular epithelial cells and CI-AKI rat models. Recombinant human STC1 (rhSTC1) regulated mitochondrial quality control, thus suppressing contrast-induced mitochondrial damage, oxidative stress, inflammatory response, and apoptotic injury. Mechanistically, activation of the Nrf2 signaling pathway contributes critically to the renoprotective effect of STC1. Together, this study demonstrates a novel role of STC1 in preventing CI-AKI and reveals Nrf2 as a molecular target of STC1. Therefore, this study provides a promising preventive target for the treatment of CI-AKI.
Highlights
Acute kidney injury has become a worldwide public health problem [1]
Our results showed that iohexol induced increased expression of dynamin-related protein 1 (Drp1), PINK1, Parkin, and LC3II and decreased expression of mfn2, TOMM20, and P62, which could be reversed by Recombinant human STC1 (rhSTC1) treatment, except the expression of LC3II and P62 (Figures 3(a) and 3(b))
Our results showed that iohexol induced increased expression of Drp1, NOD]-like pyrin domain containing protein 3 (NLRP3), high mobility group box 1 (HMGB1), PINK1, Parkin, and LC3II and decreased expression of mfn2, TOMM20, and P62, compared with the control group, which were aggravated by silencing STC1 (Figures 4(a) and 4(b))
Summary
The third most common cause of AKI is contrast medium-induced acute kidney injury which happens to 30% of patients who were administered intravascularly with contrast media [2]. CI-AKI is characterized by a sharp decrease in glomerular filtration rate (GFR) followed by an increase in serum creatinine concentration or oliguria after intravascular administration of contrast media [3, 4]. A large and growing body of researches show that CI-AKI is related to serious short- and long-term adverse outcomes, such as short-term mortality, prolonged hospitalization, increased hospital-related costs, and chronic kidney disease risk [4, 5]. A recent study shows that no prophylaxis is noninferior and cost-saving in preventing CI-AKI, compared with a common intravenous hydration prevention strategy [12]. No optional pharmaceutical has been demonstrated to effectively prevent or treat CI-AKI
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