ArticleInflammation2020
Inhibition of Proprotein Convertase Subtilisin/Kexin Type 9 Ameliorates Liver Fibrosis via Mitigation of Intestinal Endotoxemia.
Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
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
13 citing papers in PubMed, 17 citations in OpenAlex.
- Profiles of PCSK9, SREBP-2, and histopathology in COVID-19 and non-COVID-19 critical illness.BMC infectious diseases · 2025Article
- Targeting proprotein convertase subtilisin/kexin type 9 (PCSK9) to tackle central nervous system diseases: role as a promising approach.European journal of medical research · 2025Review
- PCSK9 Enhances Cardiac Fibrogenesis via the Activation of Toll-like Receptor and NLRP3 Inflammasome Signaling.International journal of molecular sciences · 2025Article
- Conditional knockdown of hepatic PCSK9 ameliorates high-fat diet-induced liver inflammation in mice.Frontiers in pharmacology · 2025Article
- Evolocumab prevents atrial fibrillation in rheumatoid arthritis rats through restraint of PCSK9 induced atrial remodeling.Journal of advanced research · 2024Article
- Review
- Anti-PCSK9 Treatment Attenuates Liver Fibrosis via Inhibiting Hypoxia-Induced Autophagy in Hepatocytes.Inflammation · 2023Article
- Effects of PCSK9 inhibitors on metabolic-associated fatty liver disease: a short review.Przeglad gastroenterologiczny · 2023Review
- Better detoxifying effect of ripe forsythiae fructus over green forsythiae fructus and the potential mechanisms involving bile acids metabolism and gut microbiota.Frontiers in pharmacology · 2022Article
- Sex difference in circulating PCSK9 and its clinical implications.Frontiers in pharmacology · 2022Review
- PCSK9 and the Gut-Liver-Brain Axis: A Novel Therapeutic Target for Immune Regulation in Alcohol Use Disorder.Journal of clinical medicine · 2021Review
- Rapid Decline of Serum Proprotein Convertase Subtilisin/Kexin 9 (PCSK9) in Non-Cirrhotic Patients with Chronic Hepatitis C Infection Receiving Direct-Acting Antiviral Therapy.Journal of clinical medicine · 2021Article
- Proprotein convertase subtilisin/kexin type 9 (PCSK9) levels are not associated with severity of liver disease and are inversely related to cholesterol in a cohort of thirty eight patients with liver cirrhosis.Lipids in health and disease · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Lipopolysaccharide (LPS) is demonstrated to cause "two-hit" injury to liver. Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays an important role in LPS clearance. Hepatocyte nuclear factor-1 alpha (HNF-1α) and sterol regulatory element-binding protein 2 (SREBP2) were reported to be responsible for PCSK9 gene transcription and regulation. We aim to clarify the expression status of PCSK9 during the process of liver fibrosis and to verify the effect on liver fibrosis via PCSK9 inhibition. In this study, we found that PCSK9 increased significantly in human and BDL mouse injured liver tissues, so did HNF-1α and SREBP2. No significant difference of plasma PCSK9 was observed. Inhibited PCSK9 using CRISPR-PCSK9 adeno-associated virus in BDL mice ameliorated liver inflammation and fibrosis, with LPS decrease in serum, without any change in intestinal wall integrity. PCSK9 expression of L02 hepatocytes can be induced by LPS; however, they lose the ability at high content of LPS. L02 cells increased LPS uptake after PCSK9 knockout. Taken together, these results suggest that, with PCSK9 increasing during liver fibrosis advancement, its inhibition can ameliorate liver injury by enhancing LPS uptake in hepatocytes; however, the enhancement is limited for destruction to hepatocytes by high LPS.
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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.