Abstract
Contrast-induced acute kidney injury (CI-AKI) is a severe complication associated with significant morbidity and mortality, and effective therapeutic strategies are still lacking. Apelin is an endogenous physiological regulator with antioxidative, anti-inflammatory and antiapoptotic properties. However, the role of apelin-13 in CI-AKI remains unclear. In our study, we found that the protein expression levels of apelin were significantly downregulated in rat kidney tissues and HK-2 cells during contrast media treatment. Moreover, we explored the protective effect of apelin-13 on renal tubule damage using in vitro and in vivo models of CI-AKI. Exogenous apelin-13 ameliorated endoplasmic reticulum stress, reactive oxygen species and apoptosis protein expression in contrast media-treated cells and rat kidney tissues. Mechanistically, the downregulation of endoplasmic reticulum stress contributed critically to the antiapoptotic effect of apelin-13. Collectively, our findings reveal the inherent mechanisms by which apelin-13 regulates CI-AKI and provide a prospective target for the prevention of CI-AKI.
Graphical Abstract
Acknowledgments
The researchers gratefully acknowledge the experimental conditions provided by Department of Nephrology, The Second Xiangya Hospital of Central South University.
Author contributions
S.B.D. conception, design, supervision and financial support. Q.L. conception, design and implementation, collection of data, data analysis and interpretation, manuscript writing. L.W. and Y.H.D. collection of data and data analysis. X.W. and X.Q.L. data analysis and manuscript writing. H.S.W., T.W., Y.X.K. and P.Y. revision of the manuscript for important intellectual content. All authors read and approved the final version of the manuscript.
Disclosure statement
The authors state no conflict of interest.
Data availability statement
The data used to support the findings of this study are available from the corresponding authors upon request.