ReviewNature reviews. Gastroenterology & hepatology2023
Antifibrotic therapy in nonalcoholic steatohepatitis: time for a human-centric approach.
Review in Nature reviews. Gastroenterology & hepatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 65 citations in OpenAlex.
- siRNA therapeutics for metabolic dysfunction-associated Steatohepatitis: Targets, delivery, clinical evidence, and translational challenges.Biochemistry and biophysics reports · 2026Review
- Liver sinusoidal endothelial cell fenestrations in metabolic liver disease: from molecular mechanisms to therapeutic perspectives.Cell communication and signaling : CCS · 2026Review
- Article
- Single-cell fixed RNA profiling uncovers SEMA4D and LMCD1 as therapeutic targets in a liver fibrosis model.JHEP reports : innovation in hepatology · 2026Article
- Senescent hepatic stellate cells drive inflammation and disease progression in MASH (Review).Experimental and therapeutic medicine · 2026Review
- Immune cells in liver injury: from pathogenic mechanisms to immunotherapy.Frontiers in immunology · 2026Review
- Review
- Association between multifactorial control and excess risk of liver diseases in type 2 diabetes: a prospective cohort study.BMJ open diabetes research & care · 2025Article
- Pharmacological manipulation of liver fibrosis progression using novel HDAC6 inhibitors.The FEBS journal · 2025Article
- Pathogenesis and Clinical Management of Metabolic Dysfunction-Associated Steatotic Liver Disease.International journal of molecular sciences · 2025Review
- AMPK activator ATX-304 reduces oxidative stress and improves MASLD via metabolic switching.JCI insight · 2025Article
- Preventing the progression of cirrhosis to decompensation and death.Nature reviews. Gastroenterology & hepatology · 2025Review
- Therapeutic landscape of metabolic dysfunction-associated steatohepatitis (MASH).Nature reviews. Drug discovery · 2025Review
- Article
- Deep learning-based method for grading histopathological liver fibrosis in rodent models of metabolic dysfunction-associated steatohepatitis.Frontiers in medicine · 2025Article
- Application of probiotic therapy in nonalcoholic fatty liver disease: mediating mechanism and future perspective.Frontiers in cellular and infection microbiology · 2025Review
- A metabolic dysfunction-associated steatotic liver acinus biomimetic induces pancreatic islet dysfunction in a coupled microphysiology system.Communications biology · 2024Article
- Metabolic Dysfunction-associated Steatotic Liver Disease and Type 2 Diabetes: A Deadly Synergy.TouchREVIEWS in endocrinology · 2024Article
- Liver Fibrosis: From Basic Science towards Clinical Progress, Focusing on the Central Role of Hepatic Stellate Cells.International journal of molecular sciences · 2024Review
- MAFLD Pandemic: Updates in Pharmacotherapeutic Approach Development.Current issues in molecular biology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 3 countries.
Funding
Abstract
Nonalcoholic steatohepatitis (NASH) might soon become the leading cause of end-stage liver disease and indication for liver transplantation worldwide. Fibrosis severity is the only histological predictor of liver-related morbidity and mortality in NASH identified to date. Moreover, fibrosis regression is associated with improved clinical outcomes. However, despite numerous clinical trials of plausible drug candidates, an approved antifibrotic therapy remains elusive. Increased understanding of NASH susceptibility and pathogenesis, emerging human multiomics profiling, integration of electronic health record data and modern pharmacology techniques hold enormous promise in delivering a paradigm shift in antifibrotic drug development in NASH. There is a strong rationale for drug combinations to boost efficacy, and precision medicine strategies targeting key genetic modifiers of NASH are emerging. In this Perspective, we discuss why antifibrotic effects observed in NASH pharmacotherapy trials have been underwhelming and outline potential approaches to improve the likelihood of future clinical success.
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.