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Signal pathways involved in contrast-induced acute kidney injury
Ke Deng1, Mingxin Pei1, Beibei Li1
1Department of Pathophysiology, Zhuhai Campus of Zunyi Medical University, Zhuhai, Guangdong, China.
Insights
Contrast-induced acute kidney injury (CI-AKI) is a major hospital concern. This review details CI-AKI pathways like inflammation and oxidative stress to guide better prevention and treatment strategies.
Area of Science:
- Nephrology
- Pathophysiology
- Molecular Biology
Background:
- Contrast-induced acute kidney injury (CI-AKI) is a significant cause of hospital-acquired kidney damage.
- CI-AKI is linked to poor patient outcomes, highlighting the need for better understanding and management.
- The exact mechanisms driving CI-AKI remain unclear, necessitating further research into its molecular underpinnings.
Purpose of the Study:
- To comprehensively review the signaling pathways involved in CI-AKI pathogenesis.
- To assess the influence of different experimental models on understanding these pathways.
- To identify improved, targeted strategies for CI-AKI prevention and treatment.
Main Methods:
- Systematic literature review of studies on CI-AKI pathophysiology.
- Analysis of signaling cascades including inflammation, oxidative stress, apoptosis, and ferroptosis.
- Evaluation of various research models used in CI-AKI studies.
Main Results:
- Multiple signaling pathways, including inflammation, oxidative stress, apoptosis, and ferroptosis, are implicated in CI-AKI.
- Interactions between these pathways contribute to the development and progression of CI-AKI.
- Research models significantly impact the interpretation of pathway analysis in CI-AKI.
Conclusions:
- Understanding the complex molecular mechanisms of CI-AKI is crucial for clinical advancement.
- Targeted interventions focusing on specific pathways show promise for preventing and treating CI-AKI.
- Further research is needed to translate mechanistic insights into effective clinical practice for CI-AKI.
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.
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