ArticleEvidence-based complementary and alternative medicine : eCAM2021
Wild Bitter Melon Extract Regulates LPS-Induced Hepatic Stellate Cell Activation, Inflammation, Endoplasmic Reticulum Stress, and Ferroptosis.
Article in Evidence-based complementary and alternative medicine : eCAM, 2021. 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
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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.
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Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- Fatty acid species differentially regulate macrophage polarization and oxidative stress with secondary effects on macrophage-HSC crosstalk.Physiological reports · 2026Article
- Endoplasmic reticulum stress-mediated cell death in spinal cord injury: from molecular mechanisms to therapeutic applications.Frontiers in cell and developmental biology · 2026Review
- Ferroptosis in liver diseases: molecular mechanisms, biomarker potential, and clinical translation.Frontiers in cell and developmental biology · 2026Review
- Endoplasmic reticulum stress sensor protein PERK in hepatic stellate cells promotes the progression of hepatocellular carcinoma via p38δ MAPK/IL-1β axis.Scientific reports · 2025Article
- SLC7A11 in Fibrosis: Molecular Mechanisms and Future Prospects.Aging and disease · 2025Review
- Advances in Understanding Lipopolysaccharide-Mediated Hepatitis: Mechanisms and Pathological Features.Current issues in molecular biology · 2025Review
- Endoplasmic Reticulum-Targeting Natural Compounds: A Novel Frontier in Alleviating Liver Fibrosis.Drug design, development and therapy · 2025Review
- ERS-PERK Pathway is Involved in the Repair of the Pulpo-Dentinal Complex Under an Inflammatory Microenvironment.Stem cells international · 2025Article
- Promising Support Coming from Nature: Antioxidant and Anti-Inflammatory Potential ofCurrent issues in molecular biology · 2024Article
- Ferroptosis in Liver Disease: Natural Active Compounds and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2024Review
- Citral-Enriched Fraction of Lemon Essential Oil Mitigates LPS-Induced Hepatocyte Injuries.Biology · 2023Article
- Zooming in and out of ferroptosis in human disease.Frontiers of medicine · 2023Review
- Iron as a therapeutic target in chronic liver disease.World journal of gastroenterology · 2023Review
- Recent progress in the effect of ferroptosis of HSCs on the development of liver fibrosis.Frontiers in molecular biosciences · 2023Review
- Endoplasmic reticulum stress-mediated cell death in liver injury.Cell death & disease · 2022Review
- Therapeutic potential of chrysin nanoparticle-mediation inhibition of succinate dehydrogenase and ubiquinone oxidoreductase in pancreatic and lung adenocarcinoma.European journal of medical research · 2022Review
- The Regulatory Roles of Polysaccharides and Ferroptosis-Related Phytochemicals in Liver Diseases.Nutrients · 2022Review
- Pharmacological modulation of ferroptosis as a therapeutic target for liver fibrosis.Frontiers in pharmacology · 2022Review
- Role of Ferroptosis in Fibrotic Diseases.Journal of inflammation research · 2022Review
- Ferroptosis in Chronic Liver Diseases: Opportunities and Challenges.Frontiers in molecular biosciences · 2022Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activation of hepatic stellate cells (HSCs) is a key component of liver fibrosis. Two antifibrosis pathways have been identified, the reversion to quiescent-type HSCs and the clearance of HSCs through apoptosis. Lipopolysaccharide- (LPS-) induced HSCs activation and proliferation have been associated with the development of liver fibrosis. We determined the pharmacological effects of wild bitter melon (WM) on HSC activation following LPS treatment and investigated whether WM treatment affected cell death pathways under LPS-treated conditions, including ferroptosis. WM treatment caused cell death, both with and without LPS treatment. WM treatment caused reactive oxygen species (ROS) accumulation without LPS treatment and reversed the decrease in lipid ROS production in HSCs after LPS treatment. We examined the effects of WM treatment on fibrosis, endoplasmic reticulum (ER) stress, inflammation, and ferroptosis in LPS-activated HSCs. The western blotting analysis revealed that the WM treatment of LPS-activated HSCs induced the downregulation of the connective tissue growth factor (CTGF),
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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.