ArticleActa pharmaceutica Sinica. B2023
Synergistic activation of AMPK by AdipoR1/2 agonist and inhibitor of EDPs-EBP interaction recover NAFLD through enhancing mitochondrial function in mice.
Article in Acta pharmaceutica Sinica. B, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- Effects of Bound Polyphenols on Lipid Metabolism in HepG2 Cells and Glucose-InducedInternational journal of molecular sciences · 2026Article
- From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis.Liver research (Beijing, China) · 2026Review
- Hyperoside modulates bile acid and fatty acid metabolism, presenting a potentially promising treatment for non-alcoholic fatty liver disease.Journal of advanced research · 2026Article
- Activating protein kinases to treat diseases: Current understanding and future challenges.Acta pharmaceutica Sinica. B · 2026Review
- Integrin β3 Orchestrates Hepatic Steatosis via a Novel CD36-Dependent Lipid Uptake Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Serum biomarker screening and metabolic profiling analysis of nonalcoholic fatty liver disease patients using untargeted metabolomics and machine learning techniques.Frontiers in molecular biosciences · 2026Article
- Urinary CFHR2 as a Biomarker for Early Diagnosis and Disease Progression Prediction in Diabetic Kidney Disease.Current molecular medicine · 2026Article
- MYD88 regulates the intercellular crosstalk landscape in MASH liver against metaflammation and metabolic disorder.Acta pharmaceutica Sinica. B · 2025Article
- NAT10 induces N4-acetylcytidine modification of AdipoR1-mediated mitochondrial biogenesis against endothelial-to-mesenchymal transition in hypertension.Molecular medicine (Cambridge, Mass.) · 2025Article
- Mitophagy as a pivotal axis in non‑alcoholic fatty liver disease: From pathogenic mechanisms to therapeutic strategies (Review).Molecular medicine reports · 2025Review
- Circular RNA circDhx32 promotes cardiac inflammatory responses in mouse cardiac ischemia-reperfusion injury via binding to FOXO1 competed with AdipoR1.Acta pharmacologica Sinica · 2025Article
- Role of adiponectin and its receptors AdipoR1/2 in inflammatory bowel disease.Cell communication and signaling : CCS · 2025Review
- Article
- New Insights into AMPK, as a Potential Therapeutic Target in Metabolic Dysfunction-Associated Steatotic Liver Disease and Hepatic Fibrosis.Biomolecules & therapeutics · 2025Review
- Research progress on AMPK in the pathogenesis and treatment of MASLD.Frontiers in immunology · 2025Review
- Adipose tissue protects against skin photodamage through CD151- and AdipoQ- EVs.Cell communication and signaling : CCS · 2024Article
- Schisanhenol ameliorates non-alcoholic fatty liver diseaseActa pharmaceutica Sinica. B · 2024Article
- Liver Cell Mitophagy in Metabolic Dysfunction-Associated Steatotic Liver Disease and Liver Fibrosis.Antioxidants (Basel, Switzerland) · 2024Review
- Drug targets regulate systemic metabolism and provide new horizons to treat nonalcoholic steatohepatitis.Metabolism open · 2024Review
- Mitophagy in fibrotic diseases: molecular mechanisms and therapeutic applications.Frontiers in physiology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic fatty liver disease (NAFLD), especially nonalcoholic steatohepatitis (NASH), is a common hepatic manifestation of metabolic syndrome. However, there are no effective therapy to treat this devastating disease. Accumulating evidence suggests that the generation of elastin-derived peptides (EDPs) and the inhibition of adiponectin receptors (AdipoR)1/2 plays essential roles in hepatic lipid metabolism and liver fibrosis. We recently reported that the AdipoR1/2 dual agonist JT003 significantly degraded the extracellular matrix (ECM) and ameliorated liver fibrosis. However, the degradation of the ECM lead to the generation of EDPs, which could further alter liver homeostasis negatively. Thus, in this study, we successfully combined AdipoR1/2 agonist JT003 with V14, which acted as an inhibitor of EDPs-EBP interaction to overcome the defect of ECM degradation. We found that combination of JT003 and V14 possessed excellent synergistic benefits on ameliorating NASH and liver fibrosis than either alone since they compensate the shortage of each other. These effects are induced by the enhancement of the mitochondrial antioxidant capacity, mitophagy, and mitochondrial biogenesis
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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.