ReviewDrug design, development and therapy2022
Biological Mechanisms and Related Natural Inhibitors of CD36 in Nonalcoholic Fatty Liver.
Review in Drug design, development and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 32 citations in OpenAlex.
- Article
- New approaches of N-acetylcysteine on fatty acid transport and metabolism in a rat model of MASLD induced by high-fat diet.Scientific reports · 2026Article
- Iturin derived fromiScience · 2026Article
- A CD36-targeted aptamer-4-butyl-polyhydroxybenzophenone conjugate with pH-responsive release for liver delivery in MASLD.Regenerative biomaterials · 2026Article
- Cedrol mitigates hepatic lipid accumulation and adipocyte hypertrophy induced by corticosteroids through the inhibition of glucocorticoid receptor activity.Scientific reports · 2025Article
- Therapeutic Potential of Quercetin, Silibinin, and Crocetin in a High-Fat Diet-Induced Mouse Model of MASLD: The Role of CD36 and PLIN3.Life (Basel, Switzerland) · 2025Article
- Engineering chimeric PCSK9 for a vaccine against atherosclerosis.Molecular therapy. Methods & clinical development · 2025Article
- Article
- Lipid Accumulation and Insulin Resistance: Bridging Metabolic Dysfunction-Associated Fatty Liver Disease and Chronic Kidney Disease.International journal of molecular sciences · 2025Review
- Conjugated Lithocholic Acid Activates Hepatic TGR5 to Promote Lipotoxicity and MASLD-MASH Transition by Disrupting Carnitine Biosynthesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- High-density lipoprotein cholesterol: how studying the 'good cholesterol' could improve cardiovascular health.Open biology · 2025Review
- Alternative splicing is an FXRα loss-of-function mechanism and impacts energy metabolism in hepatocarcinoma cells.The Journal of biological chemistry · 2025Article
- Glucuronide metabolites of trans-ε-viniferin decrease triglycerides accumulation in an in vitro model of hepatic steatosis.Journal of physiology and biochemistry · 2024Article
- Heterocyclic Amines Disrupt Lipid Homeostasis in Cryopreserved Human Hepatocytes.Cardiovascular toxicology · 2024Article
- Article
- Role of Nonalcoholic Fatty Liver Disease in Periodontitis: A Bidirectional Relationship.Cureus · 2024Review
- Examining the Pathogenesis of MAFLD and the Medicinal Properties of Natural Products from a Metabolic Perspective.Metabolites · 2024Review
- Unraveling the intricate relationship between lipid metabolism and oncogenic signaling pathways.Frontiers in cell and developmental biology · 2024Review
- Article
- Druggable targets for the immunopathy of Alzheimer's disease.RSC medicinal chemistry · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic fatty liver disease (NAFLD), a spectrum of liver disorders from non-alcoholic fatty liver (NAFL) to the more severe non-alcoholic steatohepatitis (NASH), is the leading etiology of chronic liver disease and its global prevalence is increasing. Hepatic steatosis, a condition marked by an abnormal buildup of triglycerides in the liver, is the precursor to NAFLD. Differentiated cluster 36 (CD36), a scavenger receptor class B protein, is a membrane receptor that recognizes multiple lipid and non-lipid ligands. It is generally agreed that CD36 contributes significantly to hepatic steatosis by taking part in fatty acid uptake as well as triglyceride storage and secretion. While there has not been any conclusive research on how CD36 inhibitors prevent NAFLD from progressing and no clinically approved CD36 inhibitors are currently available for use in NAFLD, CD36 remains a target worthy of further investigation in NAFLD. In recent years, the potential role of natural products acting through CD36 in treating non-alcoholic fatty liver disease has attracted much attention. This paper offers an overview of the pathogenesis of CD36 in NAFLD and summarizes some of the natural compounds or extracts that are currently being investigated for modulating NAFLD via CD36 or the CD36 pathway, providing an alternative approach to the development of CD36-related drugs in NAFLD.
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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.