ReviewCell death & disease2020
Understanding lipotoxicity in NAFLD pathogenesis: is CD36 a key driver?
Review in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 290 papers, 4 of them syntheses that pooled it.
What it found
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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
290 citing papers in PubMed, 4 syntheses or guidelines pooled it, 480 citations in OpenAlex.
- Probiotics as emerging adjuncts in metabolic associated fatty liver disease therapy-a systemic review.BMC gastroenterology · 2026Pooled it
- The role of CD36 in immune function: bridging innate and adaptive responses.Frontiers in immunology · 2026Pooled it
- Lingguizhugan Decoction in the Treatment of Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis.Endocrine, metabolic & immune disorders drug targets · 2025Pooled it
- Pooled it
- E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- Clinical outcomes of lean metabolic dysfunction-associated steatotic liver disease by phenotypic subtypes.Journal of gastroenterology · 2026Article
- Ketogenesis as a Metabolic Checkpoint in MASLD: Implications for Disease Progression and Therapy.Metabolites · 2026Review
- Article
- HFpEF and MASLD: converging mechanisms and clinical implications.Nature reviews. Cardiology · 2026Review
- Berberine Regulates Hepatic Fatty Acid Metabolism via AMPK/SIRT1/PGC-1α Pathway.Chinese journal of integrative medicine · 2026Article
- Adipose Tissue Browning in MASLD and Its Molecular Mechanisms and Metabolic Crosstalk.Current obesity reports · 2026Review
- γ-GC mitigates MASLD by reducing CD36 palmitoylation and plasma membrane translocation mediated by AKT/KLF10/zDHHC7 axis.Nutrition & metabolism · 2026Article
- Fucoxanthin Suppresses Lipid Accumulation and Inflammatory Responses in FFA-Induced Hepatocyte Models via the EGR2-CD36 Axis.Molecules (Basel, Switzerland) · 2026Article
- PLIN1 restoration modulates lipid reprogramming and impedes tumor growth in ovarian cancer.BMC cancer · 2026Article
- Technology-enabled insights into SLC transporters in MAFLD: redefining the multi-hit pathogenesis and therapeutic landscape.Acta pharmacologica Sinica · 2026Review
- Review
- Exploring Toxicological Mechanisms of Typical PFAS-Induced NAFLD through Integrated Computational Toxicology and AOP Frameworks.Environment & health (Washington, D.C.) · 2026Article
- When the Liver Flares: Inflammatory and Immunometabolic Mechanisms Driving the Transition from MASLD to MASH.Inflammation · 2026Review
- Lactobacillus johnsonii DM2420 Alleviates Dyslipidemia, Remodels Gut Microbiota, and Modulates the Intestinal CD36/SREBP1 Signaling Axis.Probiotics and antimicrobial proteins · 2026Article
- Unrevealing the Role of Flavonoids in Mitigation of Non-Alcoholic Fatty Liver Disease.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
230 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 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 common cause of chronic liver disease worldwide. NAFLD stages range from simple steatosis (NAFL) to non-alcoholic steatohepatitis (NASH) which can progress to cirrhosis and hepatocellular carcinoma. One of the crucial events clearly involved in NAFLD progression is the lipotoxicity resulting from an excessive fatty acid (FFA) influx to hepatocytes. Hepatic lipotoxicity occurs when the capacity of the hepatocyte to manage and export FFAs as triglycerides (TGs) is overwhelmed. This review provides succinct insights into the molecular mechanisms responsible for lipotoxicity in NAFLD, including ER and oxidative stress, autophagy, lipoapotosis and inflammation. In addition, we highlight the role of CD36/FAT fatty acid translocase in NAFLD pathogenesis. Up-to-date, it is well known that CD36 increases FFA uptake and, in the liver, it drives hepatosteatosis onset and might contribute to its progression to NASH. Clinical studies have reinforced the significance of CD36 by showing increased content in the liver of NAFLD patients. Interestingly, circulating levels of a soluble form of CD36 (sCD36) are abnormally elevated in NAFLD patients and positively correlate with the histological grade of hepatic steatosis. In fact, the induction of CD36 translocation to the plasma membrane of the hepatocytes may be a determining factor in the physiopathology of hepatic steatosis in NAFLD patients. Given all these data, targeting the fatty acid translocase CD36 or some of its functional regulators may be a promising therapeutic approach for the prevention and treatment of NAFLD.
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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.