High-mobility group box 1 and its related receptors: potential therapeutic targets for contrast-induced acute kidney injury

Percutaneous coronary intervention (PCI) is a crucial diagnostic and therapeutic approach for coronary heart disease. Contrast agents’ exposure during PCI is associated with a risk of contrast-induced acute kidney injury (CI-AKI). CI-AKI is characterized by a sudden decline in renal function occurri...

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Published in:International urology and nephrology 2024-07, Vol.56 (7), p.2291-2299
Main Authors: Mo, Changhua, Huang, Qili, Li, Lixia, Long, Yusheng, Shi, Ying, Lu, Zhengde, Wu, Ning, Li, Qingkuan, Zeng, Huayuan, Li, Guihua, Qiu, Lingyue, Gui, Chun, Ji, Qingwei
Format: Article
Language:English
Subjects:
Apoptosis
Cardiovascular disease
Contrast agents
Contrast media
Coronary artery disease
Cytotoxicity
Endoplasmic reticulum
Endothelial cells
Epithelial cells
Glycosylation
Heart diseases
HMGB1 protein
Hypoxia
Kidney diseases
Kidneys
Macrophages
Medicine
Medicine & Public Health
Mobility
Nephrology
Nephrology - Review
Oxidative stress
Renal function
Therapeutic targets
Toll-like receptors
Urology
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Summary:Percutaneous coronary intervention (PCI) is a crucial diagnostic and therapeutic approach for coronary heart disease. Contrast agents’ exposure during PCI is associated with a risk of contrast-induced acute kidney injury (CI-AKI). CI-AKI is characterized by a sudden decline in renal function occurring as a result of exposure to intravascular contrast agents, which is associated with an increased risk of poor prognosis. The pathophysiological mechanisms underlying CI-AKI involve renal medullary hypoxia, direct cytotoxic effects, endoplasmic reticulum stress, inflammation, oxidative stress, and apoptosis. To date, there is no effective therapy for CI-AKI. High-mobility group box 1 (HMGB1), as a damage-associated molecular pattern molecule, is released extracellularly by damaged cells or activated immune cells and binds to related receptors, including toll-like receptors and receptor for advanced glycation end product. In renal injury, HMGB1 is expressed in renal tubular epithelial cells, macrophages, endothelial cells, and glomerular cells, involved in the pathogenesis of various kidney diseases by activating its receptors. Therefore, this review provides a theoretical basis for HMGB1 as a therapeutic intervention target for CI-AKI.
ISSN:1573-2584
0301-1623
1573-2584
DOI:10.1007/s11255-024-03981-2