ArticleCell communication and signaling : CCS2019
Blockade of glycolysis-dependent contraction by oroxylin a via inhibition of lactate dehydrogenase-a in hepatic stellate cells.
Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- 6-Gingerol alleviates hepatic fibrosis via inhibiting glycolytic reprogramming by targeting IGF2BP2.Chinese herbal medicines · 2026Article
- Metabolic reprogramming in fibrosis-related diseases: underlying mechanisms and therapeutics.Molecular biomedicine · 2026Review
- Oroxylin A ameliorates hepatic steatosis and non-alcoholic fatty liver disease through the regulation of CPT1A mBiochemistry and biophysics reports · 2026Article
- 6-Shogaol inhibits HSCs activation and liver fibrosis by regulating glycolytic reprogramming via targeting HIF-1α.Chinese medicine · 2026Article
- Immunometabolic pathways in liver fibrosis: current evidence for selected plant-derived metabolites associated with traditional Chinese medicine.Frontiers in pharmacology · 2026Review
- Glycolysis to lactylation: Unraveling the metabolic and epigenetic landscape in tissue fibrosis (Review).Molecular medicine reports · 2025Review
- Advances in intrahepatic and extrahepatic vascular dysregulations in cirrhotic portal hypertension.Frontiers in medicine · 2025Review
- Inhibiting CXCR6 promotes senescence of activated hepatic stellate cells with limited proinflammatory SASP to attenuate hepatic fibrosis.Open life sciences · 2025Article
- Dual Roles of SIRT7 Inhibition by Oroxylin A Reprogram HSCs Fate: PRMT5 Succinylation-Driven Senescence and Ecto-Calreticulin-Dependent NK Cell Immune Clearance in Liver Fibrosis.Research (Washington, D.C.) · 2025Article
- Advancements in Plant-Based Therapeutics for Hepatic Fibrosis: Molecular Mechanisms and Nanoparticulate Drug Delivery Systems.International journal of molecular sciences · 2024Review
- The IGF2BP3/Notch/Jag1 pathway: A key regulator of hepatic stellate cell ferroptosis in liver fibrosis.Clinical and translational medicine · 2024Article
- Oroxylin A inhibits inflammatory cytokines in periodontitis via HO‑1.Molecular medicine reports · 2024Article
- [Research advances on the role of aerobic glycolysis in skin fibrosis diseases].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2024Review
- The mCell death & disease · 2024Article
- Network Pharmacology, Molecular Docking Analysis and Molecular Dynamics Simulation ofCurrent pharmaceutical design · 2024Article
- Hexokinase 2-mediated gene expression via histone lactylation is required for hepatic stellate cell activation and liver fibrosis.Cell metabolism · 2023Article
- Oroxylin A inhibited autoimmune hepatitis-induced liver injury and shifted Treg/Th17 balance to Treg differentiation.Experimental animals · 2023Article
- Article
- The role of hepatic microenvironment in hepatic fibrosis development.Annals of medicine · 2022Review
- Antioxidant and Hepatoprotective Effect of a Nutritional Supplement with Silymarin Phytosome, Choline Chloride, l-Cystine, Artichoke, and Vitamin E in Dogs.Antioxidants (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundContraction of hepatic stellate cells (HSCs) plays an important role in the pathogenesis of liver fibrosis by regulating sinusoidal blood flow and extracellular matrix remodeling. Here, we investigated how HSC contraction was affected by the natural compound oroxylin A, and elucidated the underlying mechanism.
methodsCell contraction and glycolysis were examined in cultured human HSCs and mouse liver fibrosis model upon oroxylin A intervention using diversified cellular and molecular assays, as well as genetic approaches.
resultsOroxylin A limited HSC contraction associated with inhibiting myosin light chain 2 phosphorylation. Oroxylin A blocked aerobic glycolysis in HSCs evidenced by reduction in glucose uptake and consumption and lactate production. Oroxylin A also decreased extracellular acidification rate and inhibited the expression and activity of glycolysis rate-limiting enzymes (hexose kinase 2, phosphofructokinase 1 and pyruvate kinas type M2) in HSCs. Then, we identified that oroxylin A blockade of aerobic glycolysis contributed to inhibition of HSC contraction. Furthermore, oroxylin A inhibited the expression and activity of lactate dehydrogenase-A (LDH-A) in HSCs, which was required for oroxylin A blockade of glycolysis and suppression of contraction. Oral administration of oroxylin A at 40 mg/kg reduced liver injury and fibrosis, and inhibited HSC glycolysis and contraction in mice with carbon tetrachloride-induced hepatic fibrosis. However, adenovirus-mediated overexpression of LDH-A significantly counteracted the oroxylin A's effects in fibrotic mice.
conclusionsBlockade of aerobic glycolysis by oroxylin A via inhibition of LDH-A reduced HSC contraction and attenuated liver fibrosis, suggesting LDH-A as a promising target for intervention of hepatic fibrosis.
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