ArticleDrug design, development and therapy2013
S-nitroso-N-acetylcysteine attenuates liver fibrosis in experimental nonalcoholic steatohepatitis.
Article in Drug design, development and therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.
What it found
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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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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
17 citing papers in PubMed, 23 citations in OpenAlex.
- Chlorogenic acid mitigates calcium oxalate monohydrate crystal-induced epithelial-to-mesenchymal transition in renal epithelial cells via suppression of HSP60 expression and p38 signaling.Cellular & molecular biology letters · 2026Article
- Potential Therapeutic Strategies for Steatosis, Oxidative Stress, Inflammation, and Fibrosis in Liver Disease.International journal of molecular sciences · 2026Review
- A Comparative Study of N-Acetyl Cysteine, Rosuvastatin, and Vitamin E in the Management of Patients with Non-Alcoholic Steatohepatitis: A Randomized Controlled Trial.Pharmaceuticals (Basel, Switzerland) · 2025Article
- The impact of aerobic and anaerobic exercise interventions on the management and outcomes of non-alcoholic fatty liver disease.Physiological research · 2024Review
- Protective role of curcumin in disease progression from non-alcoholic fatty liver disease to hepatocellular carcinoma: a meta-analysis.Frontiers in pharmacology · 2024Article
- N-Acetylcysteine and Atherosclerosis: Promises and Challenges.Antioxidants (Basel, Switzerland) · 2023Review
- Dihydroartemisinin inhibits the activation and proliferation of hepatic stellate cells by regulating miR‑29b‑3p.International journal of molecular medicine · 2023Article
- Melatonin prevents oxidative stress, inflammatory activity, and DNA damage in cirrhotic rats.World journal of gastroenterology · 2022Article
- N-Acetyl Cysteine Targets Hepatic Lipid Accumulation to Curb Oxidative Stress and Inflammation in NAFLD: A Comprehensive Analysis of the Literature.Antioxidants (Basel, Switzerland) · 2020Review
- Long term N-acetylcysteine administration rescues liver steatosis via endoplasmic reticulum stress with unfolded protein response in mice.Lipids in health and disease · 2020Article
- Heat shock protein 70 promotes lipogenesis in HepG2 cells.Lipids in health and disease · 2018Article
- Sphingosine 1-Phosphate Signaling as a Target in Hepatic Fibrosis Therapy.Frontiers in pharmacology · 2017Review
- Nitric oxide released from luminal s-nitroso-N-acetylcysteine increases gastric mucosal blood flow.Molecules (Basel, Switzerland) · 2015Article
- Hepatoprotective and Anti-fibrotic Agents: It's Time to Take the Next Step.Frontiers in pharmacology · 2015Review
- Nonalcoholic steatohepatitis: emerging targeted therapies to optimize treatment options.Drug design, development and therapy · 2015Review
- Pathogenesis of liver cirrhosis.World journal of gastroenterology · 2014Review
- Nonalcoholic Fatty liver disease: pathogenesis and therapeutics from a mitochondria-centric perspective.Oxidative medicine and cellular longevity · 2014Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S-Nitroso-N-acetylcysteine (SNAC) is a water soluble primary S-nitrosothiol capable of transferring and releasing nitric oxide and inducing several biochemical activities, including modulation of hepatic stellate cell activation. In this study, we evaluated the antifibrotic activity of SNAC in an animal model of nonalcoholic steatohepatitis (NASH) induced in Sprague-Dawley rats fed with a choline-deficient, high trans fat diet and exposed to diethylnitrosamine for 8 weeks. The rats were divided into three groups: SNAC, which received oral SNAC solution daily; NASH, which received the vehicle; and control, which received standard diet and vehicle. Genes related to fibrosis (matrix metalloproteinases [MMP]-13, -9, and -2), transforming growth factor β-1 [TGFβ-1], collagen-1α, and tissue inhibitors of metalloproteinase [TIMP-1 and -2] and oxidative stress (heat-shock proteins [HSP]-60 and -90) were evaluated. SNAC led to a 34.4% reduction in the collagen occupied area associated with upregulation of MMP-13 and -9 and downregulation of HSP-60, TIMP-2, TGFβ-1, and collagen-1α. These results indicate that oral SNAC administration may represent a potential antifibrotic treatment for NASH.
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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.