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Liver fibrosis is a major global health concern, developing as a result of chronic liver diseases (CLDs) such as viral hepatitis, alcohol-related liver disease, and non-alcoholic fatty liver disease (NAFLD). If left untreated, it can progress to cirrhosis, liver cancer, or even liver failure, significantly increasing the risk of severe complications and mortality.
Current treatment options are largely supportive, with no widely available therapies that directly target fibrosis. Research suggests that metabolic imbalances, particularly in glycolysis—the process by which cells generate energy—play a key role in disease progression.
Identifying treatments that can disrupt these pathways may offer new therapeutic strategies. One emerging approach involves targeting liver sinusoidal endothelial cell (LSEC) glycolysis, which has been linked to inflammation and fibrosis.
Quercetin: A Potential Therapeutic Approach
Quercetin, a naturally occurring flavonoid found in many fruits and vegetables, has attracted attention for its anti-inflammatory and anti-fibrotic properties. Recent studies indicate that it may influence glycolysis, a metabolic process closely linked to liver fibrosis.
By reducing the activity of key glycolytic enzymes—including hexokinase II (HK2), phosphofructokinase platelet (PFKP), and pyruvate kinase M2 (PKM2)—quercetin lowers energy production in LSECs, potentially slowing fibrosis progression.
Additionally, it reduces the secretion of CXCL1, a chemokine associated with neutrophil infiltration and inflammation. These combined effects suggest that quercetin may help address both metabolic dysfunction and inflammation, two critical drivers of liver fibrosis.
A study from Nanjing University of Chinese Medicine by Xiaoying Chen and colleagues explored quercetin’s effects using a mouse model of liver fibrosis induced by carbon tetrachloride (CCl4). The research is published in the journal Biomolecules and Biomedicine.
- Quercetin lowered levels of liver enzymes (ALT, AST) and total bile acid, markers of liver injury.
- Mice treated with quercetin also showed decreased collagen deposition and lower levels of fibrosis markers, such as hyaluronic acid and procollagen type III.
- In terms of metabolic regulation, quercetin inhibited glycolysis in LSECs, reducing lactate production, glucose consumption, and the expression of glycolytic enzymes.
- By suppressing CXCL1 secretion, quercetin decreased neutrophil infiltration, a key factor in liver fibrosis, thereby effecting inflammation control.
Implications and Future Directions
These findings highlight quercetin’s potential as a therapeutic option for liver fibrosis by addressing both metabolic dysfunction and inflammation. By inhibiting LSEC glycolysis, it may disrupt key processes that drive fibrosis progression. Additionally, its ability to reduce inflammation could help mitigate liver damage and improve overall liver function.
However, more research is needed to confirm these effects in humans. While preclinical results are promising, clinical trials will be essential to determine quercetin’s safety, effectiveness, and optimal dosing in patients with liver fibrosis. If successful, this natural compound could offer a new, targeted approach to managing liver disease, expanding treatment options beyond symptom management.
Quercetin’s role in metabolic regulation and immune modulation also raises broader questions about its potential applications in other inflammatory and metabolic disorders. Continued research could provide valuable insights into its therapeutic versatility and pave the way for more effective treatments for liver fibrosis and related conditions.
Disclaimer
The information presented in this article is based on preclinical research and should not be interpreted as medical advice. While quercetin shows promise in experimental studies, further clinical trials are necessary to establish its efficacy and safety in humans. Individuals with liver disease or other health conditions should consult a healthcare professional before considering any new treatment options.
