ArticleClinical and translational medicine2022
MD2 deficiency prevents high-fat diet-induced AMPK suppression and lipid accumulation through regulating TBK1 in non-alcoholic fatty liver disease.
Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 22 citations in OpenAlex.
- Cell Type-Specific Roles of TBK1 in Steatotic Liver Disease: Evidence for an Inflammatory TBK1Liver international : official journal of the International Association for the Study of the Liver · 2026Article
- H3K9 acetylation-dependent CHAC1 transcription in dihydroartemisinin-induced hepatic stellate cell ferroptosis.Chinese medical journal · 2026Article
- USP25 directly interacts with and deubiquitinates PPARα to increase PPARα stability in hepatocytes and attenuate high-fat diet-induced MASLD in mice.Cell death and differentiation · 2025Article
- Ganoapplanilactone C fromAntioxidants (Basel, Switzerland) · 2025Article
- TANK-Binding Kinase 1 in the Pathogenesis and Treatment of Inflammation-Related Diseases.International journal of molecular sciences · 2025Review
- Research progress on AMPK in the pathogenesis and treatment of MASLD.Frontiers in immunology · 2025Review
- Kehuang capsule inhibits MAPK and AKT signaling pathways to mitigate CClLiver research (Beijing, China) · 2024Article
- Mechanism of Metabolic Dysfunction-associated Steatotic Liver Disease: Important role of lipid metabolism.Journal of clinical and translational hepatology · 2024Review
- The cGAS-STING pathway: a therapeutic target in diabetes and its complications.Burns & trauma · 2024Review
- Article
- MD2 AMP(K)s up the link between lipid accumulation and inflammation in NAFLD.Clinical and translational medicine · 2022Article
- MD2 deficiency prevents high-fat diet-induced AMPK suppression and lipid accumulation through regulating TBK1 in non-alcoholic fatty liver disease.Clinical and translational medicine · 2022Article
- The AMPK pathway in fatty liver disease.Frontiers in physiology · 2022Review
- Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-alcoholic fatty liver disease (NAFLD) is the most predominant form of liver diseases worldwide. Recent evidence shows that myeloid differentiation factor 2 (MD2), a protein in innate immunity and inflammation, regulates liver injury in models of NAFLD. Here, we investigated a new mechanism by which MD2 participates in the pathogenesis of experimental NAFLD.
methodsWild-type, Md2
resultsTranscriptome analysis and bone marrow reconstitution studies showed that hepatocyte MD2 may participate in regulating lipid metabolism in models with NAFLD. We then discovered that Md2 deficiency in mice prevents HFD-mediated suppression of AMP-activated protein kinase (AMPK). This preservation of AMPK in Md2-deficient mice was associated with normalized sterol regulatory element binding protein 1 (SREBP1) transcriptional program and a lack of lipid accumulation in both hepatocytes and liver. We then showed that hepatocyte MD2 links HFD to AMPK/SREBP1 through TANK binding kinase 1 (TBK1). In addition, MD2-increased inflammatory factor from macrophages induces hepatic TBK1 activation and AMPK suppression.
conclusionHepatocyte MD2 plays a pathogenic role in NAFLD through TBK1-AMPK/SREBP1 and lipid metabolism pathway. These studies provide new insight into a non-inflammatory function of MD2 and evidence for the important role of MD2 in NALFD.
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