ArticleAmerican journal of physiology. Renal physiology2012
HMGB1 in renal ischemic injury.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
44 citing papers in PubMed, 85 citations in OpenAlex.
- Effects of mild hypothermia on serum HMGB1 of brain-dead donors and its impact on kidney transplantation recipients.Medicine · 2020Trial
- Targeting HMGB1 for Renal Ischemia and Reperfusion Injury: Mechanisms and Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Gut microbiota-dependent protection by Lactobacillus reuteri against renal injury in brain-dead rats.Scientific reports · 2026Article
- Myeloid Cells in Acute Kidney Injury.Seminars in nephrology · 2025Review
- Assessment of Eotaxin Concentration in Children with Chronic Kidney Disease.International journal of molecular sciences · 2025Article
- Article
- Ameliorative effect of montelukast against STZ induced diabetic nephropathy: targeting HMGB1, TLR4, NF-κB, NLRP3 inflammasome, and autophagy pathways.Inflammopharmacology · 2024Article
- High mobility group box 1 (HMGB1) mediates nicotine-induced podocyte injury.Frontiers in pharmacology · 2024Article
- Renal and Vascular Functional Decline in Aged Low Birth Weight Murine Adults.Kidney & blood pressure research · 2024Article
- The STAT1/HMGB1/NF-κB pathway in chronic inflammation and kidney injury after cisplatin exposure.Theranostics · 2023Article
- MicroRNAs in shaping the resolution phase of inflammation.Seminars in cell & developmental biology · 2022Review
- The Effect of Antioxidant Added to Preservation Solution on the Protection of Kidneys before Transplantation.International journal of molecular sciences · 2022Review
- HMGB-1 and TGFβ-1 highlight immuno-inflammatory and fibrotic processes before proteinuria onset in pediatric patients with Alport syndrome.Journal of nephrology · 2021Article
- Greater high-mobility group box 1 in male compared with female spontaneously hypertensive rats worsens renal ischemia-reperfusion injury.Clinical science (London, England : 1979) · 2020Article
- Anti-inflammatory and antioxidant activity of essential amino acid α-ketoacid analogues against renal ischemia-reperfusion damage in Wistar rats.Biomedica : revista del Instituto Nacional de Salud · 2020Article
- Ethyl Pyruvate Directly Attenuates Active Secretion of HMGB1 in Proximal Tubular Cells via Induction of Heme Oxygenase-1.Journal of clinical medicine · 2019Article
- HMGB1 redox during sepsis.Redox biology · 2017Article
- Carbon monoxide inhibits the nuclear-cytoplasmic translocation of HMGB1 in an in vitro oxidative stress injury model of mouse renal tubular epithelial cells.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2016Article
- Inflammasomes in the urinary tract: a disease-based review.American journal of physiology. Renal physiology · 2016Review
- High-mobility group box 1 inhibits HCO3- absorption in the medullary thick ascending limb through RAGE-Rho-ROCK-mediated inhibition of basolateral Na+/H+ exchange.American journal of physiology. Renal physiology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Factors that initiate cellular damage and trigger the inflammatory response cascade and renal injury are not completely understood after renal ischemia-reperfusion injury (IRI). High-mobility group box-1 protein (HMGB1) is a damage-associated molecular pattern molecule that binds to chromatin, but upon signaling undergoes nuclear-cytoplasmic translocation and release from cells. Immunohistochemical and Western blot analysis identified HMGB1 nuclear-cytoplasmic translocation and release from renal cells (particularly vascular and tubular cells) into the venous circulation after IRI. Time course analysis indicated HMGB1 release into the venous circulation progressively increased parallel to increased renal ischemic duration. Ethyl pyruvate (EP) treatment blocked H(2)O(2) (oxidative stress)-induced HMGB1 release from human umbilical vein endothelial cells in vitro, and in vivo resulted in nuclear retention and significant blunting of HMGB1 release into the circulation after IRI. EP treatment before IRI improved short-term serum creatinine and albuminuria, proinflammatory cyto-/chemokine release, and long-term albuminuria and fibrosis. The renoprotective effect of EP was abolished when exogenous HMGB1 was injected, suggesting EP's therapeutic efficacy is mediated by blocking HMGB1 translocation and release. To determine the independent effects of circulating HMGB1 after injury, exogenous HMGB1 was administered to healthy animals at pathophysiological dose. HMGB1 administration induced a rapid surge in systemic circulating cyto-/chemokines (including TNF-α, eotaxin, G-CSF, IFN-γ, IL-10, IL-1α, IL-6, IP-10, and KC) and led to mobilization of bone marrow CD34+Flk1+ cells into the circulation. Our results indicate that increased ischemic duration causes progressively enhanced HMGB1 release into the circulation triggering damage/repair signaling, an effect inhibited by EP because of its ability to block HMGB1 nuclear-cytoplasmic translocation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.