ReviewNature reviews. Gastroenterology & hepatology2021
Maladaptive regeneration - the reawakening of developmental pathways in NASH and fibrosis.
Review in Nature reviews. Gastroenterology & hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 105 citations in OpenAlex.
- Discovery of Epidermal Growth Factor-Like 7 as a Potential Non-Invasive Biomarker for Fibrosis and Mortality Risk in MASLD.Clinical and translational science · 2026Article
- The Emerging Challenge of Non-Cirrhotic MASLD-Related Hepatocellular Carcinoma: Etiology, Immunopathology, and Precision Oncology.Liver cancer · 2026Review
- The dynamic spectrum of steatotic liver disease: the global perspective.Nature reviews. Gastroenterology & hepatology · 2026Review
- From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis.Liver research (Beijing, China) · 2026Review
- Critical flaws in the molecular classification of HCC based on metabolic zonation: Letter to the editor on "Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway".Clinical and molecular hepatology · 2026Article
- Shifting cell death modes in hepatic steatosis: from apoptosis to necroptosis.Endocrine journal · 2026Review
- Spatially resolved multi-omics of human metabolic dysfunction-associated steatotic liver disease.Nature genetics · 2025Article
- MYD88 regulates the intercellular crosstalk landscape in MASH liver against metaflammation and metabolic disorder.Acta pharmaceutica Sinica. B · 2025Article
- Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025Review
- Article
- Liver immunology: Biological role and clinical significance.World journal of hepatology · 2025Review
- Inhibition of hedgehog signaling ameliorates severity of chronic pancreatitis in experimental mouse models.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Liver-specific actions of GH and IGF1 that protect against MASLD.Nature reviews. Endocrinology · 2025 · on this mapReview
- Ebastine-mediated destabilization of E3 ligase MKRN1 protects against metabolic dysfunction-associated steatohepatitis.Cellular and molecular life sciences : CMLS · 2025Article
- TGF-β1/SMAD3-mediated Non-canonical Hedgehog Signaling Promotes Pancreatic Stellate Cell Activation and Fibrosis in Chronic Pancreatitis.International journal of biological sciences · 2025Article
- Nrf1 acts as a highly-conserved determinon for maintaining robust redox homeostasis in the eco-evo-devo process of life histories.Cell stress · 2025Review
- ABL1‒YAP1 axis in intestinal stem cell activated by deoxycholic acid contributes to hepatic steatosis.Journal of translational medicine · 2024Article
- Identifying patient subgroups in MASLD and MASH-associated fibrosis: molecular profiles and implications for drug development.Scientific reports · 2024Article
- Pathogenesis and management of metabolic dysfunction-associated steatohepatitis-related hepatocellular carcinoma: a narrative review.Ewha medical journal · 2024Review
- Macrophage ATG16L1: Potential candidate for metabolic dysfunction-associated steatohepatitis treatment: Editorial on "Macrophage ATG16L1 expression suppresses metabolic dysfunction-associated steatohepatitis progression by promoting lipophagy".Clinical and molecular hepatology · 2024Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
With the rapid expansion of the obesity epidemic, nonalcoholic fatty liver disease is now the most common chronic liver disease, with almost 25% global prevalence. Nonalcoholic fatty liver disease ranges in severity from simple steatosis, a benign 'pre-disease' state, to the liver injury and inflammation that characterize nonalcoholic steatohepatitis (NASH), which in turn predisposes individuals to liver fibrosis. Fibrosis is the major determinant of clinical outcomes in patients with NASH and is associated with increased risks of cirrhosis and hepatocellular carcinoma. NASH has no approved therapies, and liver fibrosis shows poor response to existing pharmacotherapy, in part due to an incomplete understanding of the underlying pathophysiology. Patient and mouse data have shown that NASH is associated with the activation of developmental pathways: Notch, Hedgehog and Hippo-YAP-TAZ. Although these evolutionarily conserved fundamental signals are known to determine liver morphogenesis during development, new data have shown a coordinated and causal role for these pathways in the liver injury response, which becomes maladaptive during obesity-associated chronic liver disease. In this Review, we discuss the aetiology of this reactivation of developmental pathways and review the cell-autonomous and cell-non-autonomous mechanisms by which developmental pathways influence disease progression. Finally, we discuss the potential prognostic and therapeutic implications of these data for NASH and liver fibrosis.
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What Socratic 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 Socratic graph.