ArticleJHEP reports : innovation in hepatology2023
JNKs protect from cholestatic liver disease progression by modulating Apelin signalling.
Article in JHEP reports : innovation in hepatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 10 citations in OpenAlex.
- Tetramethylpyrazine modulates the Nrf2/JNK axis to intervene in ferroptosis and neuroinflammation after spinal cord injury: an integrated perspective from antioxidant to regenerative therapy.Molecular biology reports · 2026Review
- Dual targeted gene delivery strategy mediated by GalNAc-modified lipid nanoparticles enhances liver regeneration through specific knockdown of MKK4.Materials today. Bio · 2026Article
- Exceptional Uptake, Limited Protein Expression: Liver Macrophages Lost in Translation of Synthetic mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Liver B Cells Promotes MASLD Progression via the Apelin/APLNR System.International journal of medical sciences · 2025Article
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Corrections and comments
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Authors and funding
14 authors at 6 institutions in 5 countries.
Funding
Abstract
Background & Aims: Cholestatic liver injury is associated with c-Jun N-terminal kinases (JNK) activation in distinct cell types. Its hepatocyte-specific function during cholestasis, however, has not yet been established. Therefore, in our present study, we investigated the role of JNK1/2 during cholestasis and dissected its hepatocyte-specific function. Methods: A cohort of patients with primary biliary cholangitis (n = 29) and primary sclerosing cholangitis (n = 37) was examined. Wild-type, hepatocyte-specific knockout mice for Results: JNK activation was increased in liver specimens from patients with chronic cholestasis (primary biliary cholangitis and primary sclerosing cholangitis) and in livers of Conclusions: Impact and Implications: The cell-specific function of
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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 Socratic graph.