Skip to main content
SpringerLink
Log in

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

  • Nephrology - Review
  • Published:
International Urology and Nephrology Aims and scope Submit manuscript

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.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Fig. 1
Fig. 2

Similar content being viewed by others

Data availability

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

References

  1. James MT, Ghali WA, Tonelli M, Faris P, Knudtson ML, Pannu N et al (2010) Acute kidney injury following coronary angiography is associated with a long-term decline in kidney function. Kidney Int 78(8):803–809. https://doi.org/10.1038/ki.2010.258

    Article  PubMed  Google Scholar 

  2. James MT, Samuel SM, Manning MA, Tonelli M, Ghali WA, Faris P et al (2013) Contrast-induced acute kidney injury and risk of adverse clinical outcomes after coronary angiography: a systematic review and meta-analysis. Circ Cardiovasc Interv 6(1):37–43. https://doi.org/10.1161/CIRCINTERVENTIONS.112.974493

    Article  PubMed  Google Scholar 

  3. Heyman SN, Rosenberger C, Rosen S, Khamaisi M (2013) Why is diabetes mellitus a risk factor for contrast-induced nephropathy? Biomed Res Int 2013:123589. https://doi.org/10.1155/2013/123589

    Article  PubMed  PubMed Central  Google Scholar 

  4. Silvain J, Nguyen LS, Spagnoli V, Kerneis M, Guedeney P, Vignolles N et al (2018) Contrast-induced acute kidney injury and mortality in ST elevation myocardial infarction treated with primary percutaneous coronary intervention. Heart 104(9):767–772. https://doi.org/10.1136/heartjnl-2017-311975

    Article  PubMed  CAS  Google Scholar 

  5. Sun L, Zhu W, Chen X, Jiang J, Ji Y, Liu N et al (2020) Machine learning to predict contrast-induced acute kidney injury in patients with acute myocardial infarction. Front Med (Lausanne) 7:592007. https://doi.org/10.3389/fmed.2020.592007

    Article  PubMed  Google Scholar 

  6. Kim JH, Yang JH, Choi SH, Song YB, Hahn JY, Choi JH et al (2014) Predictors of outcomes of contrast-induced acute kidney injury after percutaneous coronary intervention in patients with chronic kidney disease. Am J Cardiol 114(12):1830–1835. https://doi.org/10.1016/j.amjcard.2014.09.022

    Article  PubMed  Google Scholar 

  7. Flaherty MP, Pant S, Patel SV, Kilgore T, Dassanayaka S, Loughran JH et al (2017) Hemodynamic support with a microaxial percutaneous left ventricular assist device (Impella) protects against acute kidney injury in patients undergoing high-risk percutaneous coronary intervention. Circ Res 120(4):692–700. https://doi.org/10.1161/CIRCRESAHA.116.309738

    Article  PubMed  CAS  Google Scholar 

  8. Maioli M, Toso A, Leoncini M, Gallopin M, Musilli N, Bellandi F (2012) Persistent renal damage after contrast-induced acute kidney injury: incidence, evolution, risk factors, and prognosis. Circulation 125(25):3099–3107. https://doi.org/10.1161/CIRCULATIONAHA.111.085290

    Article  PubMed  Google Scholar 

  9. Giacoppo D, Madhavan MV, Baber U, Warren J, Bansilal S, Witzenbichler B et al (2015) Impact of contrast-induced acute kidney injury after percutaneous coronary intervention on short- and long-term outcomes: pooled analysis from the HORIZONS-AMI and ACUITY trials. Circ Cardiovasc Interv 8(8):e002475. https://doi.org/10.1161/CIRCINTERVENTIONS.114.002475

    Article  PubMed  CAS  Google Scholar 

  10. Chen Q, Guan X, Zuo X, Wang J, Yin W (2016) The role of high mobility group box 1 (HMGB1) in the pathogenesis of kidney diseases. Acta Pharm Sin B 6(3):183–188. https://doi.org/10.1016/j.apsb.2016.02.004

    Article  PubMed  PubMed Central  Google Scholar 

  11. Andersson U, Tracey KJ (2011) HMGB1 is a therapeutic target for sterile inflammation and infection. Annu Rev Immunol 29:139–162. https://doi.org/10.1146/annurev-immunol-030409-101323

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  12. Yang H, Wang H, Chavan SS, Andersson U (2015) High mobility group box protein 1 (HMGB1): the prototypical endogenous danger molecule. Mol Med 21(Suppl 1):S6–S12. https://doi.org/10.2119/molmed.2015.00087

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  13. Cho E, Ko GJ (2022) The pathophysiology and the management of radiocontrast-induced nephropathy. Diagnostics (Basel) 12(1):180. https://doi.org/10.3390/diagnostics12010180

    Article  PubMed  Google Scholar 

  14. McCullough PA (2008) Contrast-induced acute kidney injury. J Am Coll Cardiol 51(15):1419–1428. https://doi.org/10.1016/j.jacc.2007.12.035

    Article  PubMed  Google Scholar 

  15. Ad-hoc working group of ERBP, Fliser D, Laville M, Covic A, Fouque D, Vanholder R, Juillard L et al (2012) A European Renal Best Practice (ERBP) position statement on the Kidney Disease Improving Global Outcomes (KDIGO) clinical practice guidelines on acute kidney injury: part 1: definitions, conservative management and contrast-induced nephropathy. Nephrol Dial Transplant 27(12):4263–4272. https://doi.org/10.1093/ndt/gfs375

    Article  Google Scholar 

  16. Seeliger E, Sendeski M, Rihal CS, Persson PB (2012) Contrast-induced kidney injury: mechanisms, risk factors, and prevention. Eur Heart J 33(16):2007–2015. https://doi.org/10.1093/eurheartj/ehr494

    Article  PubMed  Google Scholar 

  17. Sendeski MM (2011) Pathophysiology of renal tissue damage by iodinated contrast media. Clin Exp Pharmacol Physiol 38(5):292–299. https://doi.org/10.1111/j.1440-1681.2011.05503.x

    Article  PubMed  CAS  Google Scholar 

  18. Sendeski MM, Persson AB, Liu ZZ, Busch JF, Weikert S, Persson PB et al (2012) Iodinated contrast media cause endothelial damage leading to vasoconstriction of human and rat vasa recta. Am J Physiol Renal Physiol 303(12):F1592–F1598. https://doi.org/10.1152/ajprenal.00471.2012

    Article  PubMed  CAS  Google Scholar 

  19. Yang Y, Yang D, Yang D, Jia R, Ding G (2014) Role of reactive oxygen species-mediated endoplasmic reticulum stress in contrast-induced renal tubular cell apoptosis. Nephron Exp Nephrol 128(1–2):30–36. https://doi.org/10.1159/000366063

    Article  PubMed  CAS  Google Scholar 

  20. Romano G, Briguori C, Quintavalle C, Zanca C, Rivera NV, Colombo A et al (2008) Contrast agents and renal cell apoptosis. Eur Heart J 29(20):2569–2576. https://doi.org/10.1093/eurheartj/ehn197

    Article  PubMed  CAS  Google Scholar 

  21. Zhu X, Li S, Lin Q, Shao X, Wu J, Zhang W et al (2021) αKlotho protein has therapeutic activity in contrast-induced acute kidney injury by limiting NLRP3 inflammasome-mediated pyroptosis and promoting autophagy. Pharmacol Res 167:105531. https://doi.org/10.1016/j.phrs.2021.105531

    Article  PubMed  CAS  Google Scholar 

  22. Dai B, Su Q, Liu X, Mi X, Dou L, Zhou D et al (2023) 2, 2-dimethylthiazolidine hydrochloride protects against experimental contrast-induced acute kidney injury via inhibition of tubular ferroptosis. Biochem Biophys Res Commun 679:15–22. https://doi.org/10.1016/j.bbrc.2023.08.052

    Article  PubMed  CAS  Google Scholar 

  23. Liu X, Li Q, Sun L, Chen L, Li Y, Huang B et al (2021) miR-30e-5p regulates autophagy and apoptosis by targeting Beclin1 involved in contrast-induced acute kidney injury. Curr Med Chem 28(38):7974–7984. https://doi.org/10.2174/0929867328666210526125023

    Article  PubMed  CAS  Google Scholar 

  24. Seeliger E, Flemming B, Wronski T, Ladwig M, Arakelyan K, Godes M et al (2007) Viscosity of contrast media perturbs renal hemodynamics. J Am Soc Nephrol 18(11):2912–2920. https://doi.org/10.1681/ASN.2006111216

    Article  PubMed  CAS  Google Scholar 

  25. Kim K, Jeong B, Lee YM, Son HE, Ryu JY, Park S et al (2022) Three-dimensional kidney-on-a-chip assessment of contrast-induced kidney injury: osmolality and viscosity. Micromachines (Basel) 13(5):688. https://doi.org/10.3390/mi13050688

    Article  PubMed  Google Scholar 

  26. Li Q, Pan S (2022) Contrast-associated acute kidney injury: advances and challenges. Int J Gen Med 15:1537–1546. https://doi.org/10.2147/IJGM.S341072

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  27. Heyman SN, Rosen S, Khamaisi M, Idée JM, Rosenberger C (2010) Reactive oxygen species and the pathogenesis of radiocontrast-induced nephropathy. Invest Radiol 45(4):188–195. https://doi.org/10.1097/RLI.0b013e3181d2eed8

    Article  PubMed  Google Scholar 

  28. Cheng AS, Li X (2023) The potential biotherapeutic targets of contrast-induced acute kidney injury. Int J Mol Sci 24(9):8254. https://doi.org/10.3390/ijms24098254

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  29. Heyman SN, Rosen S, Rosenberger C (2008) Renal parenchymal hypoxia, hypoxia adaptation, and the pathogenesis of radiocontrast nephropathy. Clin J Am Soc Nephrol 3(1):288–296. https://doi.org/10.2215/CJN.02600607

    Article  PubMed  Google Scholar 

  30. Yang Z, Qiao Y, Wang D, Yan G, Tang C (2023) Association between inflammatory biomarkers and contrast-induced acute kidney injury in ACS patients undergoing percutaneous coronary intervention: a cross-sectional study. Angiology 19:33197231185445. https://doi.org/10.1177/00033197231185445

    Article  Google Scholar 

  31. Machado RA, Constantino Lde S, Tomasi CD, Rojas HA, Vuolo FS, Vitto MF et al (2012) Sodium butyrate decreases the activation of NF-κB reducing inflammation and oxidative damage in the kidney of rats subjected to contrast-induced nephropathy. Nephrol Dial Transplant 27(8):3136–3140. https://doi.org/10.1093/ndt/gfr807

    Article  PubMed  CAS  Google Scholar 

  32. Bianchi ME, Falciola L, Ferrari S, Lilley DM (1992) The DNA binding site of HMG1 protein is composed of two similar segments (HMG boxes), both of which have counterparts in other eukaryotic regulatory proteins. EMBO J 11(3):1055–1063. https://doi.org/10.1002/j.1460-2075.1992.tb05144.x

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  33. Li J, Kokkola R, Tabibzadeh S, Yang R, Ochani M, Qiang X et al (2003) Structural basis for the proinflammatory cytokine activity of high mobility group box 1. Mol Med 9(1–2):37–45

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  34. Cai J, Wen J, Bauer E, Zhong H, Yuan H, Chen AF (2015) The role of HMGB1 in cardiovascular biology: danger signals. Antioxid Redox Signal 23(17):1351–1369. https://doi.org/10.1089/ars.2015.6408

    Article  PubMed  CAS  Google Scholar 

  35. Yang H, Ochani M, Li J, Qiang X, Tanovic M, Harris HE et al (2004) Reversing established sepsis with antagonists of endogenous high-mobility group box 1. Proc Natl Acad Sci USA 101(1):296–301. https://doi.org/10.1073/pnas.2434651100

    Article  ADS  PubMed  CAS  Google Scholar 

  36. Stros M (1998) DNA bending by the chromosomal protein HMG1 and its high mobility group box domains. Effect of flanking sequences. J Biol Chem 273(17):10355–10361

    Article  PubMed  CAS  Google Scholar 

  37. Wang Q, Zeng M, Wang W, Tang J (2007) The HMGB1 acidic tail regulates HMGB1 DNA binding specificity by a unique mechanism. Biochem Biophys Res Commun 360(1):14–19. https://doi.org/10.1016/j.bbrc.2007.05.130

    Article  PubMed  CAS  Google Scholar 

  38. Liu T, Li Q, Jin Q, Yang L, Mao H, Qu P et al (2023) Targeting HMGB1: a potential therapeutic strategy for chronic kidney disease. Int J Biol Sci 19(15):5020–5035. https://doi.org/10.7150/ijbs.87964

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  39. Carta S, Castellani P, Delfino L, Tassi S, Venè R, Rubartelli A (2009) DAMPs and inflammatory processes: the role of redox in the different outcomes. J Leukoc Biol 86(3):549–555. https://doi.org/10.1189/jlb.1008598

    Article  PubMed  CAS  Google Scholar 

  40. Yang H, Antoine DJ, Andersson U, Tracey KJ (2013) The many faces of HMGB1: molecular structure-functional activity in inflammation, apoptosis, and chemotaxis. J Leukoc Biol 93(6):865–873. https://doi.org/10.1189/jlb.1212662

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  41. Bonaldi T, Talamo F, Scaffidi P, Ferrera D, Porto A, Bachi A et al (2003) Monocytic cells hyperacetylate chromatin protein HMGB1 to redirect it towards secretion. EMBO J 2(20):5551–5560. https://doi.org/10.1093/emboj/cdg516

    Article  Google Scholar 

  42. Ito I, Fukazawa J, Yoshida M (2007) Post-translational methylation of high mobility group box 1 (HMGB1) causes its cytoplasmic localization in neutrophils. J Biol Chem 282(22):16336–16344. https://doi.org/10.1074/jbc.M608467200

    Article  PubMed  CAS  Google Scholar 

  43. Youn JH, Shin JS (2006) Nucleocytoplasmic shuttling of HMGB1 is regulated by phosphorylation that redirects it toward secretion. J Immunol 177(11):7889–7897. https://doi.org/10.4049/jimmunol.177.11.7889

    Article  PubMed  CAS  Google Scholar 

  44. Scaffidi P, Misteli T, Bianchi ME (2002) Release of chromatin protein HMGB1 by necrotic cells triggers inflammation. Nature 418(6894):191–195. https://doi.org/10.1038/nature00858

    Article  ADS  PubMed  CAS  Google Scholar 

  45. Kazama H, Ricci JE, Herndon JM, Hoppe G, Green DR, Ferguson TA (2008) Induction of immunological tolerance by apoptotic cells requires caspase-dependent oxidation of high-mobility group box-1 protein. Immunity 29(1):21–32. https://doi.org/10.1016/j.immuni.2008.05.013

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  46. Matsuura R, Komaru Y, Miyamoto Y, Yoshida T, Yoshimoto K, Yamashita T et al (2023) HMGB1 is a prognostic factor for mortality in acute kidney injury requiring renal replacement therapy. Blood Purif 52(7–8):660–667. https://doi.org/10.1159/000530774

    Article  PubMed  CAS  Google Scholar 

  47. Lau A, Wang S, Liu W, Haig A, Zhang ZX, Jevnikar AM (2014) Glycyrrhizic acid ameliorates HMGB1-mediated cell death and inflammation after renal ischemia reperfusion injury. Am J Nephrol 40(1):84–95. https://doi.org/10.1159/000364908

    Article  PubMed  CAS  Google Scholar 

  48. Zhao Z, Hu Z, Zeng R, Yao Y (2020) HMGB1 in kidney diseases. Life Sci 259:118203. https://doi.org/10.1016/j.lfs.2020.118203

    Article  PubMed  CAS  Google Scholar 

  49. Zhang C, Dong H, Chen F, Wang Y, Ma J, Wang G (2019) The HMGB1-RAGE/TLR-TNF-α signaling pathway may contribute to kidney injury induced by hypoxia. Exp Ther Med 17(1):17–26. https://doi.org/10.3892/etm.2018.6932

    Article  PubMed  CAS  Google Scholar 

  50. Miura K, Sahara H, Sekijima M, Kawai A, Waki S, Nishimura H et al (2014) Protective effect of neutralization of the extracellular high-mobility group box 1 on renal ischemia-reperfusion injury in miniature swine. Transplantation 98(9):937–943. https://doi.org/10.1097/TP.0000000000000358

    Article  PubMed  CAS  Google Scholar 

  51. Wang Y, Zhang H, Chen Q, Jiao F, Shi C, Pei M et al (2020) TNF-α/HMGB1 inflammation signalling pathway regulates pyroptosis during liver failure and acute kidney injury. Cell Prolif 53(6):e12829. https://doi.org/10.1111/cpr.12829

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  52. Guan XF, Chen QJ, Zuo XC, Guo R, Peng XD, Wang JL et al (2017) Contrast media-induced renal inflammation is mediated through HMGB1 and its receptors in human tubular cells. DNA Cell Biol 36(1):67–76. https://doi.org/10.1089/dna.2016.3463

    Article  PubMed  CAS  Google Scholar 

  53. Neyra JA, Chawla LS (2021) Acute kidney disease to chronic kidney disease. Crit Care Clin 37(2):453–474. https://doi.org/10.1016/j.ccc.2020.11.013

    Article  PubMed  Google Scholar 

  54. Venkatachalam MA, Weinberg JM, Kriz W, Bidani AK (2015) Failed tubule recovery, AKI-CKD transition, and kidney disease progression. J Am Soc Nephrol 26(8):1765–1776. https://doi.org/10.1681/ASN.2015010006

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  55. Zhao ZB, Marschner JA, Iwakura T, Li C, Motrapu M, Kuang M et al (2023) Tubular epithelial cell HMGB1 promotes AKI-CKD transition by sensitizing cycling tubular cells to oxidative stress: a rationale for targeting HMGB1 during AKI recovery. J Am Soc Nephrol 34(3):394–411. https://doi.org/10.1681/ASN.0000000000000024

    Article  PubMed  PubMed Central  Google Scholar 

  56. Tanaka S, Tanaka T, Nangaku M (2014) Hypoxia as a key player in the AKI-to-CKD transition. Am J Physiol Renal Physiol 307(11):F1187–F1195. https://doi.org/10.1152/ajprenal.00425.2014

    Article  PubMed  CAS  Google Scholar 

  57. Mo C, Ma X, Jian W, Huang Q, Zheng W, Yang Z et al (2022) High mobility group box 1 and homocysteine as preprocedural predictors for contrast-induced acute kidney injury after percutaneous coronary artery intervention. Int Urol Nephrol 54(7):1663–1671. https://doi.org/10.1007/s11255-021-03050-y

    Article  PubMed  CAS  Google Scholar 

  58. Oh H, Choi A, Seo N, Lim JS, You JS, Chung YE (2021) Protective effect of glycyrrhizin, a direct HMGB1 inhibitor, on post-contrast acute kidney injury. Sci Rep 11(1):15625. https://doi.org/10.1038/s41598-021-94928-5

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  59. Zhao H, Liu Z, Shen H, Jin S, Zhang S (2016) Glycyrrhizic acid pretreatment prevents sepsis-induced acute kidney injury via suppressing inflammation, apoptosis and oxidative stress. Eur J Pharmacol 781:92–99. https://doi.org/10.1016/j.ejphar.2016.04.006

    Article  PubMed  CAS  Google Scholar 

  60. Sohn EJ, Kang DG, Lee HS (2003) Protective effects of glycyrrhizin on gentamicin-induced acute renal failure in rats. Pharmacol Toxicol 93(3):116–122. https://doi.org/10.1034/j.1600-0773.2003.930302.x

    Article  PubMed  CAS  Google Scholar 

  61. Thakur V, Nargis S, Gonzalez M, Pradhan S, Terreros D, Chattopadhyay M (2017) Role of glycyrrhizin in the reduction of inflammation in diabetic kidney disease. Nephron 137(2):137–147. https://doi.org/10.1159/000477820

    Article  PubMed  CAS  Google Scholar 

  62. Yue RZ, Li YJ, Su BH, Li CJ, Zeng R (2023) Atorvastatin reduces contrast media-induced pyroptosis of renal tubular epithelial cells by inhibiting the TLR4/MyD88/NF-κB signaling pathway. BMC Nephrol 24(1):25. https://doi.org/10.1186/s12882-023-03066-9

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  63. Awad AM, Elshaer SL, Gangaraju R, Abdelaziz RR, Nader MA (2023) Ameliorative effect of montelukast against STZ induced diabetic nephropathy: targeting HMGB1, TLR4, NF-κB, NLRP3 inflammasome, and autophagy pathways. Inflammopharmacology. https://doi.org/10.1007/s10787-023-01301-1

    Article  PubMed  PubMed Central  Google Scholar 

  64. Shen J, Wang L, Jiang N, Mou S, Zhang M, Gu L et al (2016) NLRP3 inflammasome mediates contrast media-induced acute kidney injury by regulating cell apoptosis. Sci Rep 6:34682. https://doi.org/10.1038/srep34682

    Article  ADS  PubMed  PubMed Central  CAS  Google Scholar 

  65. Luo M, Liu Z, Hu Z, He Q (2022) Quercetin improves contrast-induced acute kidney injury through the HIF-1α/lncRNA NEAT1/HMGB1 pathway. Pharm Biol 60(1):889–898. https://doi.org/10.1080/13880209.2022.2058558

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  66. Shelke V, Kale A, Dagar N, Habshi T, Gaikwad AB (2023) Concomitant inhibition of TLR-4 and SGLT2 by phloretin and empagliflozin prevents diabetes-associated ischemic acute kidney injury. Food Funct 14(11):5391–5403. https://doi.org/10.1039/d3fo01379k

    Article  PubMed  CAS  Google Scholar 

  67. Katare PB, Nizami HL, Paramesha B, Dinda AK, Banerjee SK (2020) Activation of toll like receptor 4 (TLR4) promotes cardiomyocyte apoptosis through SIRT2 dependent p53 deacetylation. Sci Rep 10(1):19232. https://doi.org/10.1038/s41598-020-75301-4

    Article  ADS  PubMed  PubMed Central  CAS  Google Scholar 

  68. Zhou S, Lu S, Guo S, Zhao L, Han Z, Li Z (2021) Protective effect of ginsenoside Rb1 nanoparticles against contrast-induced nephropathy by inhibiting high mobility group box 1 Gene/toll-Like receptor 4/NF-κB signaling pathway. J Biomed Nanotechnol 17(10):2085–2098. https://doi.org/10.1166/jbn.2021.3163

    Article  PubMed  CAS  Google Scholar 

  69. Huang Q, Yang Z, Zhou JP, Luo Y (2017) HMGB1 induces endothelial progenitor cells apoptosis via RAGE-dependent PERK/eIF2α pathway. Mol Cell Biochem 431(1–2):67–74. https://doi.org/10.1007/s11010-017-2976-2

    Article  PubMed  CAS  Google Scholar 

  70. He F, Gu L, Cai N, Ni J, Liu Y, Zhang Q et al (2022) The HMGB1-RAGE axis induces apoptosis in acute respiratory distress syndrome through PERK/eIF2α/ATF4-mediated endoplasmic reticulum stress. Inflamm Res 71(10–11):1245–1260. https://doi.org/10.1007/s00011-022-01613-y

    Article  PubMed  CAS  Google Scholar 

  71. Kim S, Joe Y, Surh YJ, Chung HT (2018) Differential regulation of toll-like receptor-mediated cytokine production by unfolded protein response. Oxid Med Cell Longev 2018:9827312. https://doi.org/10.1155/2018/9827312

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  72. Ferrè S, Deng Y, Huen SC, Lu CY, Scherer PE, Igarashi P et al (2019) Renal tubular cell spliced X-box binding protein 1 (Xbp1s) has a unique role in sepsis-induced acute kidney injury and inflammation. Kidney Int 96(6):1359–1373. https://doi.org/10.1016/j.kint.2019.06.023

    Article  PubMed  PubMed Central  Google Scholar 

  73. Liu J, Huang K, Cai GY, Chen XM, Yang JR, Lin LR et al (2014) Receptor for advanced glycation end-products promotes premature senescence of proximal tubular epithelial cells via activation of endoplasmic reticulum stress-dependent p21 signaling. Cell Signal 26(1):110–121. https://doi.org/10.1016/j.cellsig.2013.10.002

    Article  PubMed  CAS  Google Scholar 

  74. Lai HJ, Zhan YQ, Qiu YX, Ling YH, Zhang XY, Chang ZN et al (2021) HMGB1 signaling-regulated endoplasmic reticulum stress mediates intestinal ischemia/reperfusion-induced acute renal damage. Surgery 170(1):239–248. https://doi.org/10.1016/j.surg.2021.01.042

    Article  PubMed  Google Scholar 

  75. Zhang J, Chen Q, Dai Z, Pan H (2023) miR-22 alleviates sepsis-induced acute kidney injury via targeting the HMGB1/TLR4/NF-κB signaling pathway. Int Urol Nephrol 55(2):409–421. https://doi.org/10.1007/s11255-022-03321-2

    Article  PubMed  CAS  Google Scholar 

  76. Michel HE, Menze ET (2019) Tetramethylpyrazine guards against cisplatin-induced nephrotoxicity in rats through inhibiting HMGB1/TLR4/NF-κB and activating Nrf2 and PPAR-γ signaling pathways. Eur J Pharmacol 857:172422. https://doi.org/10.1016/j.ejphar.2019.172422

    Article  PubMed  CAS  Google Scholar 

  77. Zhang GZ, Zhang K, Yang SQ, Zhang Z, Chen S, Hou BJ et al (2020) VASPIN reduces inflammation and endoplasmic reticulum stress of renal tubular epithelial cells by inhibiting HMGB1 and relieves renal ischemia-reperfusion injury. Eur Rev Med Pharmacol Sci 24(17):8968–8977. https://doi.org/10.26355/eurrev_202009_22839.

  78. Shelke V, Kale A, Anders HJ, Gaikwad AB (2023) Toll-like receptors 2 and 4 stress signaling and sodium-glucose cotransporter-2 in kidney disease. Mol Cell Biochem 478(9):1987–1998. https://doi.org/10.1007/s11010-022-04652-5

    Article  PubMed  CAS  Google Scholar 

  79. Zhang M, Guo Y, Fu H, Hu S, Pan J, Wang Y et al (2015) Chop deficiency prevents UUO-induced renal fibrosis by attenuating fibrotic signals originated from Hmgb1/TLR4/NFκB/IL-1β signaling. Cell Death Dis 6(8):e1847. https://doi.org/10.1038/cddis.2015.206

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  80. Zeng KW, Zhang T, Fu H, Liu GX, Wang XM (2012) Schisandrin B exerts anti-neuroinflammatory activity by inhibiting the Toll-like receptor 4-dependent MyD88/IKK/NF-κB signaling pathway in lipopolysaccharide-induced microglia. Eur J Pharmacol 692(1–3):29–37. https://doi.org/10.1016/j.ejphar.2012.05.030

    Article  PubMed  CAS  Google Scholar 

  81. Sun Y, Peng PA, Ma Y, Liu XL, Yu Y, Jia S et al (2017) Valsartan protects against contrast-induced acute kidney injury in rats by inhibiting endoplasmic reticulum stress-induced apoptosis. Curr Vasc Pharmacol 15(2):174–183. https://doi.org/10.2174/1570161114666161025100656

    Article  PubMed  CAS  Google Scholar 

  82. Peng PA, Wang L, Ma Q, Xin Y, Zhang O, Han HY et al (2015) Valsartan protects HK-2 cells from contrast media-induced apoptosis by inhibiting endoplasmic reticulum stress. Cell Biol Int 39(12):1408–1417. https://doi.org/10.1002/cbin.10521

    Article  PubMed  CAS  Google Scholar 

Download references

Acknowledgements

We thank Dr. Xiao Ma from the First Affiliated Hospital of Guangxi Medical University for his kind support in reviewing the manuscript for integrity check and giving precious opinions.

Funding

This work was supported by the National Natural Science Foundation of China (No. 82260060 to Dr. Qingwei Ji).

Author information

Author notes

  1. Changhua Mo and Qili Huang contributed equally to this work.

Authors and Affiliations

  1. Department of Cardiology, The People’s Hospital of Guangxi Zhuang Autonomous Region and Research Center of Cardiovascular Disease, Guangxi Academy of Medical Sciences, Nanning, China

    Changhua Mo, Qili Huang, Lixia Li, Yusheng Long, Ying Shi, Zhengde Lu, Ning Wu, Qingkuan Li, Huayuan Zeng, Guihua Li, Lingyue Qiu & Qingwei Ji

  2. Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University and Guangxi Key Laboratory Base of Precision Medicine in Cardiocerebrovascular Diseases Control and Prevention and Guangxi Clinical Research Center for Cardiocerebrovascular Diseases, Nanning, China

    Chun Gui

Authors
  1. Changhua Mo
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Qili Huang
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Lixia Li
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Yusheng Long
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Ying Shi
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Zhengde Lu
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Ning Wu
    View author publications

    You can also search for this author in PubMed Google Scholar

  8. Qingkuan Li
    View author publications

    You can also search for this author in PubMed Google Scholar

  9. Huayuan Zeng
    View author publications

    You can also search for this author in PubMed Google Scholar

  10. Guihua Li
    View author publications

    You can also search for this author in PubMed Google Scholar

  11. Lingyue Qiu
    View author publications

    You can also search for this author in PubMed Google Scholar

  12. Chun Gui
    View author publications

    You can also search for this author in PubMed Google Scholar

  13. Qingwei Ji
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

Manuscript designing and outlining: Changhua Mo, Gui Chun, and Qingwei Ji; manuscript writing: Changhua Mo and Qili Huang; figure and table creating: Changhua Mo, Lixia Li, Yusheng Long, Guihua Li, and Lingyue Qiu; and clinical consulting and revision: Ying Shi, Zhengde Lu, Ning Wu, Qingkuan Li, and Huayuan Zeng. All the authors read the submitted version and approved it.

Corresponding authors

Correspondence to Chun Gui or Qingwei Ji.

Ethics declarations

Conflict of interest

The authors declare no conflicts of interest with the contents of this article.

Ethical approval

Not applicable.

Consent to participate

Not applicable.

Consent for publication

Not applicable.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Mo, C., Huang, Q., Li, L. et al. High-mobility group box 1 and its related receptors: potential therapeutic targets for contrast-induced acute kidney injury. Int Urol Nephrol (2024). https://doi.org/10.1007/s11255-024-03981-2

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1007/s11255-024-03981-2

Keywords

Search

Navigation