ReviewFrontiers in physiology2018
The Biological Clock: A Pivotal Hub in Non-alcoholic Fatty Liver Disease Pathogenesis.
Review in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05618626 (Cardiovascular Diseases), which is not on this map. Cited by 35 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.
Cardiovascular Diseases (CVD) and Nonalcoholic Fatty Liver Diseases (NAFLD) Among Gallstone and Cholecystectomy Patients and the Impact of a Novel Diet and Muscle Training Program
Who cites it
35 citing papers in PubMed, 59 citations in OpenAlex.
- Review
- Liver clock: Malalignment and entrainment therapeutics.World journal of gastrointestinal pharmacology and therapeutics · 2026Review
- Role of SIRT3 in digestive system diseases and therapeutic prospects (Review).International journal of molecular medicine · 2026Review
- The Multifaceted Role of Cytochrome P450 Isoenzymes in Alcoholic and Metabolic (Dysfunction) Fatty Liver Diseases.Current drug metabolism · 2026Review
- Associations Between Shift Work, Sociodemographic and Lifestyle Characteristics, Body Measurements, and MASLD.Life (Basel, Switzerland) · 2025Article
- Dynamic crosstalk between HSCs and liver microenvironment: multicellular interactions in the regulation of liver fibrosis.Frontiers in cell and developmental biology · 2025Review
- Cilostazol Attenuates Hepatic Steatosis and Intestinal Disorders in Nonalcoholic Fatty Liver Disease.International journal of molecular sciences · 2024Article
- Early but Not Late Exercise Training in Mice Exacerbates Hepatic Inflammation in Developing Nonalcoholic Fatty Liver Disease.Journal of clinical and translational hepatology · 2023Article
- Review
- Experimental Data on the Role of Melatonin in the Pathogenesis of Nonalcoholic Fatty Liver Disease.Biomedicines · 2023Review
- Effect of Circadian Rhythm Disturbance on the Human Musculoskeletal System and the Importance of Nutritional Strategies.Nutrients · 2023Review
- Is Fasting Good When One Is at Risk of Liver Cancer?Cancers · 2022Review
- Article
- The gut microbial metabolite, 3,4-dihydroxyphenylpropionic acid, alleviates hepatic ischemia/reperfusion injuryActa pharmaceutica Sinica. B · 2022Article
- Attenuation by Time-Restricted Feeding of High-Fat and High-Fructose Diet-Induced NASH in Mice Is Related to Per2 and Ferroptosis.Oxidative medicine and cellular longevity · 2022Article
- The Histone Variant MacroH2A1 Impacts Circadian Gene Expression and Cell Phenotype in an In Vitro Model of Hepatocellular Carcinoma.Biomedicines · 2021Article
- Article
- Oral Pathobiont-Induced Changes in Gut Microbiota Aggravate the Pathology of Nonalcoholic Fatty Liver Disease in Mice.Frontiers in immunology · 2021Article
- Blood Pressure Model Based on Hybrid Feature Convolution Neural Network in Promoting Rehabilitation of Patients with Hypertensive Intracerebral Hemorrhage.Computational and mathematical methods in medicine · 2021Article
- Unraveling the Role of Leptin in Liver Function and Its Relationship with Liver Diseases.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most frequent hepatic pathology in the Western world and may evolve into steatohepatitis (NASH), increasing the risk of cirrhosis, portal hypertension and hepatocellular carcinoma. NAFLD derives from the accumulation of hepatic fat due to discrepant free fatty acid metabolism. Other factors contributing to this are deranged nutrients and bile acids fluxes as well as alterations in nuclear receptors, hormones, and intermediary metabolites, which impact on signaling pathways involved in metabolism and inflammation. Autophagy and host gut-microbiota interplay are also relevant to NAFLD pathogenesis. Notably, liver metabolic pathways and bile acid synthesis as well as autophagic and immune/inflammatory processes all show circadian patterns driven by the biological clock. Gut microbiota impacts on the biological clock, at the same time as the appropriate timing of metabolic fluxes, hormone secretion, bile acid turnover, autophagy and inflammation with behavioural cycles of fasting/feeding and sleeping/waking is required to circumvent hepatosteatosis, indicating significant interactions of the gut and circadian processes in NAFLD pathophysiology. Several time-related factors and processes interplay in NAFLD development, with the biological clock proposed to act as a network level hub. Deranged physiological rhythms (chronodisruption) may also play a role in liver steatosis pathogenesis. The current article reviews how the circadian clock circuitry intimately interacts with several mechanisms involved in the onset of hepatosteatosis and its progression to NASH, thereby contributing to the global NAFLD epidemic.
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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.