ReviewHandbook of experimental pharmacology2019
Pharmacologic Modulation of Bile Acid-FXR-FGF15/FGF19 Pathway for the Treatment of Nonalcoholic Steatohepatitis.
Review in Handbook of experimental pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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
31 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Bile Acids and FXR: Novel Targets for Liver Diseases.Frontiers in medicine · 2020Pooled it
- LECT2 deficiency contributes to bile acid metabolic reprogramming and cholestatic liver injury.Hepatology communications · 2026Article
- Mechanisms and therapeutic insights into MASH-associated fibrosis.Trends in endocrinology and metabolism: TEM · 2026Review
- FXR in bone metabolism: An emerging regulator.iScience · 2026Review
- Gut microbiome and bile acid metabolism in liver disease: Mechanisms, clinical implications, and therapeutic opportunities.Pharmacological reviews · 2026Review
- LC2767 alleviates LPS-induced liver injury and fibrosis by regulating FXR expression, NF-κB activation, and gut microbiota.Scientific reports · 2026Article
- Gut microbiota in non-alcoholic fatty liver disease: Pathophysiology, diagnosis, and therapeutics.World journal of hepatology · 2025Review
- Ursodeoxycholic acid acts as an ileal FXR agonist in male mice with hepatic deficiency of FXR.eGastroenterology · 2025Article
- Liver-gut axis signaling regulates circadian energy metabolism in shift workers.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Potential therapeutic strategies for MASH: from preclinical to clinical development.Life metabolism · 2024Review
- FXR Agonism with Bile Acid Mimetic Reduces Pre-Clinical Triple-Negative Breast Cancer Burden.Cancers · 2024Article
- Targeting nuclear receptors for NASH/MASH: From bench to bedside.Liver research (Beijing, China) · 2024Article
- Bile Acid Diarrhea: From Molecular Mechanisms to Clinical Diagnosis and Treatment in the Era of Precision Medicine.International journal of molecular sciences · 2024Review
- Benefits of CombiningFoods (Basel, Switzerland) · 2023Review
- Treatment of liver fibrosis: Past, current, and future.World journal of hepatology · 2023Review
- Ginsenoside Rh4 Improves Hepatic Lipid Metabolism and Inflammation in a Model of NAFLD by Targeting the Gut Liver Axis and Modulating the FXR Signaling Pathway.Foods (Basel, Switzerland) · 2023Article
- Fibroblast growth factor 19 secretion and function in perinatal development.American journal of physiology. Gastrointestinal and liver physiology · 2023Review
- Review
- Bile acid and receptors: biology and drug discovery for nonalcoholic fatty liver disease.Acta pharmacologica Sinica · 2022Review
- Pleiotropic roles of FXR in liver and colorectal cancers.Molecular and cellular endocrinology · 2022Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Nonalcoholic steatohepatitis (NASH) is within the spectrum of nonalcoholic fatty liver disease (NAFLD) and can progress to fibrosis, cirrhosis, and even hepatocellular carcinoma (HCC). The prevalence of NASH is rising and has become a large burden to the medical system worldwide. Unfortunately, despite its high prevalence and severe health consequences, there is currently no therapeutic agent approved to treat NASH. Therefore, the development of efficacious therapies is of utmost urgency and importance. Many molecular targets are currently under investigation for their ability to halt NASH progression. One of the most promising and well-studied targets is the bile acid (BA)-activated nuclear receptor, farnesoid X receptor (FXR). In this chapter, the characteristics, etiology, and prevalence of NASH will be discussed. A brief introduction to FXR regulation of BA homeostasis will be described. However, for more details regarding FXR in BA homeostasis, please refer to previous chapters. In this chapter, the mechanisms by which tissue and cell type-specific FXR regulates NASH development will be discussed in detail. Several FXR agonists have reached later phase clinical trials for treatment of NASH. The progress of these compounds and summary of released data will be provided. Lastly, this chapter will address safety liabilities specific to the development of FXR agonists.
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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.