ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2012
Opposing roles of RAGE and Myd88 signaling in extensive liver resection.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- PathwayKO: An integrated platform for deciphering the systems-level signaling pathways.Frontiers in immunology · 2023Article
- Inflammation Meets Metabolism: Roles for the Receptor for Advanced Glycation End Products Axis in Cardiovascular Disease.Immunometabolism · 2021Article
- Empathy in stroke rats is modulated by social settings.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Receptor for Advanced Glycation End Products (RAGE) and Mechanisms and Therapeutic Opportunities in Diabetes and Cardiovascular Disease: Insights From Human Subjects and Animal Models.Frontiers in cardiovascular medicine · 2020Review
- Exclusive enteral nutrition protects against inflammatory bowel disease by inhibiting NF‑κB activation through regulation of the p38/MSK1 pathway.International journal of molecular medicine · 2018Article
- Liver Regeneration in the Acute Liver Failure Patient.Clinics in liver disease · 2018Review
- 22016 ATVB Plenary Lecture: Receptor for Advanced Glycation Endproducts and Implications for the Pathogenesis and Treatment of Cardiometabolic Disorders: Spotlight on the Macrophage.Arteriosclerosis, thrombosis, and vascular biology · 2017Review
- Glycation & the RAGE axis: targeting signal transduction through DIAPH1.Expert review of proteomics · 2017Review
- Identifying biologically relevant putative mechanisms in a given phenotype comparison.PloS one · 2017Article
- Small Molecule Inhibition of Ligand-Stimulated RAGE-DIAPH1 Signal Transduction.Scientific reports · 2016Article
- The multiple faces of RAGE--opportunities for therapeutic intervention in aging and chronic disease.Expert opinion on therapeutic targets · 2016Review
- Soluble RAGEs - Prospects for treating & tracking metabolic and inflammatory disease.Vascular pharmacology · 2015Review
- Role of the receptor for advanced glycation endproducts (RAGE) in retinal vasodegenerative pathology during diabetes in mice.Diabetologia · 2015Article
- Role of receptor for advanced glycation end products (RAGE) in liver disease.European journal of medical research · 2015Review
- Measurement of methylglyoxal by stable isotopic dilution analysis LC-MS/MS with corroborative prediction in physiological samples.Nature protocols · 2014Article
- Article
- RAGE deficiency improves postinjury sciatic nerve regeneration in type 1 diabetic mice.Diabetes · 2013Article
- Receptor for advanced glycation end products (RAGE) and implications for the pathophysiology of heart failure.Current heart failure reports · 2012Review
- The diverse ligand repertoire of the receptor for advanced glycation endproducts and pathways to the complications of diabetes.Vascular pharmacologyReview
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
In extensive liver resection secondary to primary or metastatic liver tumors, or in living donor liver transplantation, strategies to quell deleterious inflammatory responses and facilitate regeneration are essential. The receptor for advanced glycation endproducts (RAGE) and myeloid differentiating factor 88 (Myd88) are implicated in the inflammatory response. To establish the contributions of RAGE vs. Myd88 signaling in extensive liver resection, we probed the effect of RAGE and/or Myd88, the latter primarily a key transducer of major toll-like receptors and also implicated in interleukin-1 (Il1) signaling, in a murine model of extensive (85%) hepatectomy. We report that, although Myd88 is thoroughly essential for survival via regulation of NF-κB and TNF-α, deletion of RAGE significantly improved survival compared to wild-type, Myd88-null, or RAGE-null/Myd88-null mice. RAGE opposes Myd88 signaling at multiple levels: by suppression of p65 levels, thereby reducing activation of NF-κB and consequent production of cyclin D1, and by suppression of Il6-mediated phosphorylation of Stat3, thereby down-regulating Pim1 and suppressing the hyperplastic response. Further, RAGE-dependent suppression of glyoxalase1, a detoxification pathway for pre-AGEs, enhances AGE levels and suppresses Il6 action. We conclude that blockade of RAGE may rescue liver remnants from the multiple signals that preclude adaptive proliferation triggered primarily by Myd88 signaling pathways.
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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.