ReviewJACC. Basic to translational science2025
The Cardiohepatic Axis in Metabolic Disease: Liver to Heart.
Review in JACC. Basic to translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Early Cardiotoxic Remodelling Precedes Hepatic Fibrosis and Increases Susceptibility to Lethal Arrhythmias in Wild-Type MASH Mice.Clinical and experimental pharmacology & physiology · 2026Article
- Associations Between Domestic Water Hardness, Genetic Risk and Severe MASLD: A Large-Scale Cohort Study.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Metabolic signatures and machine learning identify gut-liver-heart axis dysfunction as a potential link to major adverse cardiovascular events in coronary artery disease.Cardiovascular diabetology. Endocrinology reports · 2026Article
- The MASLD-Cardio-Oncology Triangle: Dietary Patterns, Metabolic Remodelling and Implications for Cancer Therapy Tolerance.Nutrients · 2026Review
- Unifying and unique roles of non-coding RNA biomarkers in liver and heart fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Review
- Dehydrocostus lactone attenuates hepatic steatosis by regulating fatty acid oxidation and lipid metabolism: integrated transcriptomic and metabolomic analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The Liver-Testis Axis: Molecular Mechanisms and Clinical Implications.International journal of molecular sciences · 2026Review
- Suppression of Post-Ischemic Cardiac Remodelling and Inflammatory Response by a Novel Sphingolipid Modifier, CIN038.International journal of molecular sciences · 2026Article
- Article
- Pillars of Peer Review.JACC. Basic to translational science · 2026Article
- Ursodeoxycholic acid as a potential cardioprotective agent: molecular mechanisms, experimental evidence, and clinical perspectives.Frontiers in pharmacology · 2026Review
- Link between Metabolic Dysfunction-Associated Steatotic Liver Disease and Cardiovascular Diseases.Research (Washington, D.C.) · 2026Review
- Joint associations of lipoprotein(a) and systemic inflammatory indices with FibroTouch-derived hepatic steatosis and liver stiffness in Chinese adults.Frontiers in immunology · 2026Article
- Serum uric acid-to-high-density lipoprotein cholesterol ratio and cardiovascular risk in Asian patients with metabolic dysfunction-associated steatotic liver disease.World journal of gastroenterology · 2025Article
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.
Funding
Abstract
Heart and liver metabolic diseases often coexist because of local and systemic disorders that affect both organs via cardio-hepatic interactions. Here, we discuss the emerging evidence of organ crosstalk during cardiometabolic disease with an emphasis on the liver-to-heart axis. We highlight potential mechanisms by which metabolic dysfunction-associated steatotic liver disease contributes to cardiovascular complications. Metabolic dysfunction-associated steatotic liver disease, particularly its inflammatory entity, leads to the production of liver-derived secretory factors that regulate cardiac metabolism, inflammation, and remodeling. Thus, secreted hepatic factors represent an important mechanism of communication between the liver and heart during cardiometabolic disease. In addition to the direct crosstalk between organs, we argue that bone marrow reprogramming and clonal hematopoiesis of indeterminate potential are shared mechanisms of systemic inflammation that regulate the heart-liver axis during cardiometabolic disease. Thus, integrated cardiometabolic strategies hold a significant potential to bridge the gap between liver and cardiovascular health to improve patient outcomes.
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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.