Redox biologyJun 24, 2019

The PINK1-parkin system protects kidneys from contrast dye injury by reducing mitochondrial stress and inflammation

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Feb 10, 2026

Abstract

More than 30% of patients experience contrast-induced acute kidney injury (CI-AKI) after intravenous iodinated contrast media.

Mitophagy was induced in renal tubular epithelial cells during CI-AKI, observed both in living organisms and in laboratory settings.
Silencing PINK1 or PARK2 abolished contrast media-induced mitophagy, highlighting the importance of the PINK1-Parkin pathway.
PINK1- or PARK2-deficient cells and mice showed more severe mitochondrial damage, increased mitochondrial reactive oxygen species (ROS), and greater renal injury compared to normal groups.
PINK1-Parkin-mediated mitophagy may prevent apoptosis of renal tubular epithelial cells and reduce tissue damage by lowering mitochondrial ROS and NLRP3 inflammasome activation.

Simplified

Contrast-induced acute kidney injury (CI-AKI) occurs in more than 30% of patients after intravenous iodinated contrast media and causes serious complications, including renal failure and mortality. Recent research has demonstrated that routine antioxidant and alkaline therapy failed to show benefits in CI-AKI patients with high risk for renal complications. Mitophagy is a mechanism of selective autophagy, which controls mitochondrial quality and mitochondrial reactive oxygen species (ROS) through degradation of damaged mitochondria. The role of mitophagy and its regulation of apoptosis in CI-AKI are poorly understood. In this study, we demonstrated that mitophagy was induced in renal tubular epithelial cells (RTECs) during CI-AKI, both in vivo and in vitro. Meanwhile, contrast media-induced mitophagy was abolished when silencing PINK1 or PARK2 (Parkin), indicating a dominant role of the PINK1-Parkin pathway in mitophagy. Moreover, mitochondrial damage, mitochondrial ROS, RTEC apoptosis, and renal injury under contrast exposure were more severe in PINK1- or PARK2-deficient cells and mice than in wild-type groups. Functionally, PINK1-Parkin-mediated mitophagy prevented RTEC apoptosis and tissue damage in CI-AKI through reducing mitochondrial ROS and subsequent NLRP3 inflammasome activation. These results demonstrated that PINK1-Parkin-mediated mitophagy played a protective role in CI-AKI by reducing NLRP3 inflammasome activation.

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The PINK1-parkin system protects kidneys from contrast dye injury by reducing mitochondrial stress and inflammation

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