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Review
. 2024 Nov 25:15:1490725.
doi: 10.3389/fphys.2024.1490725. eCollection 2024.

Signal pathways involved in contrast-induced acute kidney injury

Ke Deng  1 , Mingxin Pei  1 , Beibei Li  1 , Nanqi Yang  1 , Zijian Wang  1 , Xinchi Wan  1 , Zhiying Zhong  1 , Zhiyi Yang  1 , Yanling Chen  1
Affiliations
Review

Signal pathways involved in contrast-induced acute kidney injury

Ke Deng et al. Front Physiol. .

Abstract

Contrast-induced acute kidney injury (CI-AKI) has emerged as a global public health concern, ranking as the third most prevalent cause of hospital-acquired acute kidney injury, which is related to adverse outcomes. However, its precise pathogenesis remains elusive. Consequently, researchers are dedicated to uncovering CI-AKI's pathophysiology and signaling pathways, including inflammation, oxidative stress, apoptosis, and ferroptosis, to improve prevention and treatment. This review thoroughly analyzes the signaling pathways and their interactions associated with CI-AKI, assesses the impact of various research models on pathway analysis, and explores more precise targeted treatment and prevention approaches. Aims to furnish a robust theoretical foundation for the molecular mechanisms underpinning clinical treatments.

Keywords: apoptosis; contrast-induced acute kidney injury; ferroptosis; inflammation; oxidative stress; signal pathways.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Pathophysiological mechanism of CI-AKI. There are three main aspects of the mechanism of CI-AKI genesis that are currently generally recognized. Firstly, CM can cause apoptosis, necrosis, pyroptosis, inflammatory response, and ferroptosis through direct cytotoxicity; in addition, CM promotes the generation and release of ROS and thus leads to oxidative stress; and CM can cause renal vasoconstriction and inhibit the production of NO, PG, and other vasodilating active ingredients, which leads to ischemia and hypoxia injury, and ultimately leads to renal impairment in combination with the other two mechanisms.
FIGURE 2
FIGURE 2
Oxidative stress pathways in CI-AKI. CM induces NOX activation and upregulates NOX4 expression, while aberrant NOX activation promotes eNOS dysregulation and uncoupling, leading to decrease NO bioavailability, superoxide production and ONOO-formation, and consequently aggravates endothelial dysfunction with decreased NO release and elevated ROS production. CM also induces PKC phosphorylation through the AMPK/PKC pathway, which controls NOX activation and eNOS uncoupling, leading to oxidative stress and endothelial damage. CM also reduces nrf2 expression, which inhibits HO-1 transcriptional activation, leading to an increase in eNOS production and prolonged oxidative stress. In addition, CM further increases ROS production by decreasing the expression of oxidative stress protective factors such as SIRT1, SIRT3, PGC-1α and dephosphorylated FoxO1, triggering oxidative stress.
FIGURE 3
FIGURE 3
Signal Pathways Involved in contrast-induced acute kidney injury. This figure summarizes the main pathways Involved in the mechanism of CI-AKI.
See this image and copyright information in PMC

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