ArticleCell reports. Medicine2025
Hepato-cardiac interorgan communication controls cardiac hypertrophy via combined endocrine-autocrine FGF21 signaling.
Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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
6 citing papers in PubMed.
- Mitochondrial Distress Signals at the Heart-Liver Interface: Molecular Links Between MASLD and Heart Failure.International journal of molecular sciences · 2026Review
- Decoding the mechanistic basis of liver-muscle communication in health and disease.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- International Utah cardiac recovery symposium (U-CARS) 2025:translational and basic science proceedings.Heart failure reviews · 2026Review
- Heart-Specific and Conditional Deletion of theCells · 2026Article
- Cross-trait genomic modeling reveals the polygenic architecture and systemic impact of MASLD.Science advances · 2026Article
- DWORF Gene Therapy Improves Cardiac Calcium Handling and Mitochondrial Function.Circulation research · 2025Article
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Fibroblast growth factor (FGF) 21 is a hormone produced mainly by the liver but also other organs, including the heart. Although FGF21 analogs are used for treating obesity and metabolic syndrome in humans, preclinical and clinical studies have elicited mixed results about whether prolonged FGF21 signaling is protective or detrimental for cardiac function. Based on our findings, showing elevated serum and cardiac FGF21 levels in humans with increased left ventricular afterload, we explore the involvement of FGF21 in cardiac hypertrophy. Our mouse studies reveal interorgan liver-heart crosstalk, which is controlled by an initial hepatic FGF21 release followed by the induction of cardiomyocyte (CM) FGF21 expression. Tissue-specific genetic ablation or anti-sense oligonucleotide-based inhibition of FGF21 shows that, in response to pressure overload, CM FGF21 upregulation is a critical event that is stimulated by liver-derived FGF21 and drives cardiac hypertrophy likely by interfering with cardioprotective oxytocin signaling. Conclusively, the hepato-cardiac FGF21-based signaling axis governs cardiac hypertrophy.
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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.