ReviewFrontiers in endocrinology2022
Regulatory network and interplay of hepatokines, stellakines, myokines and adipokines in nonalcoholic fatty liver diseases and nonalcoholic steatohepatitis.
Review in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers, 1 of them a synthesis that pooled it.
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
21 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Correlations between circulating adipokines and hepatocellular carcinoma: a Systematic Review and meta-analysis.Frontiers in endocrinology · 2025Pooled it
- Exploring the Molecular Mechanism of Cinnamaldehyde Intervening in Ochratoxin A-Induced Type 2 Diabetes Mellitus and Non-Alcoholic Fatty Liver Disease Comorbidity: An Integrated Approach Based on Network Pharmacology, Network Toxicology and Molecular Docking.Pharmaceuticals (Basel, Switzerland) · 2026Article
- The Liver-Heart Axis in Rheumatoid Arthritis: Associations of Liver Fibrosis, Organokines, Endothelin-1, and Cardiovascular Risk.International journal of molecular sciences · 2026Article
- Review
- The Serpin Superfamily in Adipose Tissue Remodeling: Molecular Drivers of Immune-Metabolic Crosstalk and Insulin Sensitivity.Biology · 2026Review
- Elevated FIB-4 index as a risk marker within the KDIGO framework in patients with type 2 diabetes and hypertension.BMJ open diabetes research & care · 2026Article
- From Adipose Dysfunction to Multi-Organ Steatosis: Defining the Metabolic Steatotic Axis.Current issues in molecular biology · 2026Review
- Liver steatosis, selected organokines, and cardiovascular risk markers in rheumatoid arthritis.Frontiers in endocrinology · 2026Article
- Analysis of risk factors and correlation between the degree of hepatic steatosis and fibrosis in patients with metabolic dysfunction-associated steatohepatitis.BMC gastroenterology · 2025Article
- Research advances in traditional Chinese medicine formulae and active components targeting lipid metabolism for hepatocellular carcinoma therapy.Frontiers in pharmacology · 2025Review
- From adiposity to steatosis: metabolic dysfunction-associated steatotic liver disease, a hepatic expression of metabolic syndrome - current insights and future directions.Clinical diabetes and endocrinology · 2024Review
- Lower muscular strength is associated with greater liver fat content and higher serum liver enzymes-"The Sedentary's Liver" The Study of Health in Pomerania.European journal of sport science · 2024Article
- Underlying Mechanisms behind the Brain-Gut-Liver Axis and Metabolic-Associated Fatty Liver Disease (MAFLD): An Update.International journal of molecular sciences · 2024Review
- Drug targets regulate systemic metabolism and provide new horizons to treat nonalcoholic steatohepatitis.Metabolism open · 2024Review
- Circular RNAs, Noncoding RNAs, and N6-methyladenosine Involved in the Development of MAFLD.Non-coding RNA · 2024Review
- Gliclazide Reduces Colitis-Associated Colorectal Cancer Formation by Deceasing Colonic Inflammation and Regulating AMPK-NF-κB Signaling Pathway.Digestive diseases and sciences · 2024Article
- Involvement of the vagus nerve and hepatic gene expression in serum adiponectin concentrations in mice.Journal of physiology and biochemistry · 2024Article
- Signaling pathways that activate hepatic stellate cells during liver fibrosis.Frontiers in medicine · 2024Review
- U-Shaped relationship of insulin-like growth factor I and incidence of nonalcoholic fatty liver in patients with pituitary neuroendocrine tumors: a cohort study.Frontiers in endocrinology · 2024Article
- Anti-osteoporotic treatments in the era of non-alcoholic fatty liver disease: friend or foe.Frontiers in endocrinology · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
Abstract
Fatty liver disease is a spectrum of liver pathologies ranging from simple hepatic steatosis to non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), and culminating with the development of cirrhosis or hepatocellular carcinoma (HCC). The pathogenesis of NAFLD is complex and diverse, and there is a lack of effective treatment measures. In this review, we address hepatokines identified in the pathogenesis of NAFLD and NASH, including the signaling of FXR/RXR, PPARα/RXRα, adipogenesis, hepatic stellate cell activation/liver fibrosis, AMPK/NF-κB, and type 2 diabetes. We also highlight the interaction between hepatokines, and cytokines or peptides secreted from muscle (myokines), adipose tissue (adipokines), and hepatic stellate cells (stellakines) in response to certain nutritional and physical activity. Cytokines exert autocrine, paracrine, or endocrine effects on the pathogenesis of NAFLD and NASH. Characterizing signaling pathways and crosstalk amongst muscle, adipose tissue, hepatic stellate cells and other liver cells will enhance our understanding of interorgan communication and potentially serve to accelerate the development of treatments for NAFLD and NASH.
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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.