ReviewJHEP reports : innovation in hepatology2026
The use of FGF21 analogues in MASH and MASH cirrhosis - metabolic master regulators or liver-specific mechanisms?
Review in JHEP reports : innovation in hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Metabolic Dysfunction-Associated Steatotic Disease and Genetic Risk in Germany-An Observational Real-World Cohort Study.United European gastroenterology journal · 2026Observational
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor 21 (FGF21) is a pleiotropic endocrine hormone that coordinates metabolic homeostasis across the liver, adipose tissue, pancreas, and central nervous system. In metabolic dysfunction-associated steatotic liver disease (MASLD), circulating FGF21 levels are markedly elevated, yet downstream signalling remains blunted - a state of FGF21 resistance driven by reduced β-klotho co-receptor availability and altered receptor complex function. Pharmacological FGF21 analogues were engineered to overcome the unfavourable pharmacokinetics of native FGF21 and achieve sustained target engagement at the FGFR1c/β-klotho complex in key tissues. Liver-directed effects of FGF21 analogues encompass suppression of de novo lipogenesis and lipotoxic intermediates, attenuation of hepatocellular stress and innate immune activation, and inhibition of hepatic stellate cell activation. Systemically, FGF21 signalling remodels adipose tissue via the FGF21-adiponectin axis, reduces atherogenic dyslipidaemia, improves insulin sensitivity, and modulates central pathways of energy expenditure and macronutrient preference. This breadth of action positions FGF21 analogues as both metabolic master regulators and liver-directed therapeutics. In phase II clinical trials, efruxifermin, pegozafermin, and efimosfermin have demonstrated meaningful histological improvements in patients with fibrotic metabolic dysfunction-associated steatohepatitis (MASH). In addition, efruxifermin has been shown to promote histological regression of cirrhosis in a dedicated trial of patients with compensated cirrhosis. Phase III programmes are now underway to establish their effects on liver-related outcomes and mortality. FGF21 analogues appear particularly potent in inducing fibrosis regression despite only modest weight loss, supporting a complementary combination strategy. Current evidence supports FGF21 pathway activation as a meaningful strategy to modify MASH progression and potentially reverse cirrhotic liver disease.
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Registered trials
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