ArticleHepatology (Baltimore, Md.)2017
Syndecan-1 limits the progression of liver injury and promotes liver repair in acetaminophen-induced liver injury in mice.
Article in Hepatology (Baltimore, Md.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Deletion of Pleiotrophin protects against high-fat diet-induced liver metabolic disease, independently of the sexual dimorphism in dietary response.Molecular biomedicine · 2026Article
- Analysis of the prognostic efficacy of syndecan-1 for patients with ACLF and its functional role in liver regeneration.BMC medicine · 2025Article
- Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics.Signal transduction and targeted therapy · 2025Review
- Heparan sulfate chains in hepatocellular carcinoma.Gastroenterology report · 2025Review
- Syndecan-1: a key player in health and disease.Immunogenetics · 2024Review
- Acetaminophen overdose-induced acute liver injury can be alleviated by static magnetic field.Zoological research · 2024Article
- EGR1 is crucial for the chlorogenic acid-provided promotion on liver regeneration and repair after APAP-induced liver injury.Cell biology and toxicology · 2023Article
- Sulfated motifs in heparan sulfate inhibitProteoglycan research · 2023Article
- Article
- Evaluating the immunogenicity of heparin and heparin derivatives by measuring their binding to platelet factor 4 using biolayer interferometry.Frontiers in molecular biosciences · 2022Article
- Improving the Sensitivity for Quantifying Heparan Sulfate from Biological Samples.Analytical chemistry · 2021Article
- Ulinastatin protects against acetaminophen-induced liver injury by alleviating ferroptosis via the SIRT1/NRF2/HO-1 pathway.American journal of translational research · 2021Article
- Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage.Biomedicines · 2020Review
- Host syndecan-1 promotes listeriosis by inhibiting intravascular neutrophil extracellular traps.PLoS pathogens · 2020Article
- Syndecan-1 in Liver Diseases.Pathology oncology research : POR · 2020Article
- Design of anti-inflammatory heparan sulfate to protect against acetaminophen-induced acute liver failure.Science translational medicine · 2020Article
- An Unexpected Role of Cholesterol Sulfotransferase and its Regulation in Sensitizing Mice to Acetaminophen-Induced Liver Injury.Molecular pharmacology · 2019Article
- Role and mechanisms of autophagy in acetaminophen-induced liver injury.Liver international : official journal of the International Association for the Study of the Liver · 2018Review
- The role of apoptosis in acetaminophen hepatotoxicity.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2018Review
- Dietary α-Mangostin Provides Protective Effects against Acetaminophen-Induced Hepatotoxicity in Mice via Akt/mTOR-Mediated Inhibition of Autophagy and Apoptosis.International journal of molecular sciences · 2018Article
Corrections and comments
- Commented on by
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Accidental or intentional misuse of acetaminophen (APAP) is the leading cause of acute liver failure in the Western world. Although mechanisms that trigger APAP-induced liver injury (AILI) are well known, those that halt the progression of APAP liver disease and facilitate liver recovery are less understood. Heparan sulfate proteoglycans (HSPGs) bind to and regulate various tissue injury factors through their heparan sulfate (HS) chains, but the importance of HSPGs in liver injury in vivo remains unknown. Here, we examined the role of syndecan-1, the major cell-surface HSPG of hepatocytes, in AILI. Ablation of syndecan-1 in mice led to unopposed progression of liver injury upon APAP overdose. However, direct APAP hepatoxicity and liver injury at early times post-APAP overdose were unaffected by syndecan-1, suggesting that syndecan-1 influences later mechanisms that lead to liver repair. The exuberant liver injury phenotypes in syndecan-1 null (Sdc1
conclusionThese results demonstrate that 2-O-sulfated domains in syndecan-1 HS halt disease progression and promote liver repair by enhancing hepatocyte survival in AILI. We propose that syndecan-1 is a critical endogenous factor that controls the balance between prosurvival signaling and apoptosis in hepatocytes in APAP liver disease. (Hepatology 2017;66:1601-1615).
Indexed as
Identifiers
What OpenQuestion holds
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.