High-mobility group box 1 and its related receptors: potential therapeutic targets for contrast-induced acute kidney injury
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Updated: May 5, 2026

An Effective Mouse Model of Unilateral Renal Ischemia-Reperfusion Injury
Published on: July 15, 2021
Changhua Mo1, Qili Huang1, Lixia Li1
1Department of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region and Research Center of Cardiovascular Disease, Guangxi Academy of Medical Sciences, Nanning, China.
Insights
Contrast agents used in percutaneous coronary intervention (PCI) can cause acute kidney injury (AKI). High-mobility group box 1 (HMGB1) may be a new therapeutic target for preventing contrast-induced AKI (CI-AKI).
Area of Science:
- Nephrology
- Cardiology
- Molecular Biology
Background:
- Percutaneous coronary intervention (PCI) is vital for coronary heart disease but carries a risk of contrast-induced acute kidney injury (CI-AKI).
- CI-AKI significantly increases morbidity and mortality, with no current effective treatments.
- Pathophysiological mechanisms include renal hypoxia, cellular stress, inflammation, and apoptosis.
Purpose of the Study:
- To review the role of High-mobility group box 1 (HMGB1) in CI-AKI pathogenesis.
- To explore HMGB1 as a potential therapeutic target for CI-AKI.
Main Methods:
- Literature review of studies on CI-AKI and HMGB1.
- Analysis of HMGB1 expression and function in renal injury models.
- Examination of HMGB1 receptor interactions in the context of CI-AKI.
Main Results:
- HMGB1 is implicated in the pathogenesis of various kidney diseases, including CI-AKI.
- HMGB1 is released by damaged cells and activates inflammatory pathways via its receptors.
- HMGB1 is expressed in multiple renal cell types involved in CI-AKI.
Conclusions:
- HMGB1 plays a significant role in the development of CI-AKI.
- Targeting HMGB1 presents a promising therapeutic strategy for preventing and treating CI-AKI.
- Further research into HMGB1-targeted therapies is warranted for CI-AKI management.
Abstract:
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.
Related Concept Videos
Acute Kidney Injury I: Introduction
Acute Kidney Injury II: Pathophysiology
Acute Kidney Injury III: Clinical Manifestations
Acute Kidney Injury IV: Diagnostic Studies and Prevention
Acute Kidney Injury V: Interprofessional Care
Acute Kidney Injury VI: Nursing Management

