ArticleLaboratory investigation; a journal of technical methods and pathology2011
Cytokines induce small intestine and liver injury after renal ischemia or nephrectomy.
Article in Laboratory investigation; a journal of technical methods and pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 181 citations in OpenAlex.
- Effects of low versus standard pressure pneumoperitoneum on renal syndecan-1 shedding and VEGF receptor-2 expression in living-donor nephrectomy: a randomized controlled study.BMC anesthesiology · 2020Trial
- Brazilin attenuates kidney ischemia-reperfusion injury by regulating inflammation, oxidative stress, and mitochondrial dysfunction.Histology and histopathology · 2026Article
- FTY-720 pre-treatment attenuates acute lung injury following bilateral renal ischemia/reperfusion but not bilateral nephrectomy.Scientific reports · 2026Article
- Burns: The "Fuse" That Ignites Organ Crisis - A Narrative Review of Mechanisms and Crosstalk in Post-Burn MODS.Journal of inflammation research · 2026Review
- Clostridium scindens attenuates acute kidney injury by producing indole-3-acetic acid.NPJ biofilms and microbiomes · 2025Article
- Identification of diagnostic biomarkers and mitochondrial metabolic characteristics in sepsis-associated acute kidney injury.European journal of medical research · 2025Article
- Hepato-Renal Crosstalk in Acute and Chronic Disease: From Shared Pathways to Therapeutic Targets.Biomedicines · 2025Review
- Development and validation of a predictive model for postoperative hepatic dysfunction in Stanford type A aortic dissection.Scientific reports · 2025Article
- Fecal microbiota transplantation is a promising therapy for kidney diseases.Frontiers in medicine · 2025Review
- Lymphocytes and innate immune cells in acute kidney injury and repair.Nature reviews. Nephrology · 2024Review
- Incidence, risk factors, and outcomes of acute liver injury in hospitalized adults with acute kidney injury: a large multicenter study.Hepatology international · 2024Article
- Disruption in glutathione metabolism and altered energy production in the liver and kidney after ischemic acute kidney injury in mice.Scientific reports · 2024Article
- Review on Kidney-Liver Crosstalk: Pathophysiology of Their Disorders.Cell journal · 2024Article
- Interorgan communication networks in the kidney-lung axis.Nature reviews. Nephrology · 2024Review
- Recent insights into contributing factors in the pathogenesis of cirrhotic ascites.Frontiers in medicine · 2024Review
- Heart-gut microbiota communication determines the severity of cardiac injury after myocardial ischaemia/reperfusion.Cardiovascular research · 2023Article
- Mineralocorticoid Receptor Antagonism Attenuates Multiple Organ Failure after Renal Ischemia and Reperfusion in Mice.International journal of molecular sciences · 2023Article
- Article
- Intestinal microbiota dysbiosis in acute kidney injury: novel insights into mechanisms and promising therapeutic strategies.Renal failure · 2022Review
- Effect of Renal Ischemia Reperfusion on Brain Neuroinflammation.Biomedicines · 2022Article
18 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
Patients with acute kidney injury (AKI) frequently suffer from extra-renal complications including hepatic dysfunction and systemic inflammation. We aimed to determine the mechanisms of AKI-induced hepatic dysfunction and systemic inflammation. Mice subjected to AKI (renal ischemia reperfusion (IR) or nephrectomy) rapidly developed acute hepatic dysfunction and suffered significantly worse hepatic IR injury. After AKI, rapid peri-portal hepatocyte necrosis, vacuolization, neutrophil infiltration and pro-inflammatory mRNA upregulation were observed suggesting an intestinal source of hepatic injury. Small intestine histology after AKI showed profound villous lacteal capillary endothelial apoptosis, disruption of vascular permeability and epithelial necrosis. After ischemic or non-ischemic AKI, plasma TNF-α, IL-17A and IL-6 increased significantly. Small intestine appears to be the source of IL-17A, as IL-17A levels were higher in the portal circulation and small intestine compared with the levels measured from the systemic circulation and liver. Wild-type mice treated with neutralizing antibodies against TNF-α, IL-17A or IL-6 or mice deficient in TNF-α, IL-17A, IL-17A receptor or IL-6 were protected against hepatic and small intestine injury because of ischemic or non-ischemic AKI. For the first time, we implicate the increased release of IL-17A from small intestine together with induction of TNF-α and IL-6 as a cause of small intestine and liver injury after ischemic or non-ischemic AKI. Modulation of the inflammatory response and cytokine release in the small intestine after AKI may have important therapeutic implications in reducing complications arising from AKI.
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