ArticleBritish journal of pharmacology2012
Azelnidipine is a calcium blocker that attenuates liver fibrosis and may increase antioxidant defence.
Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- Effects of azelnidipine, a calcium channel blocker, in a rat femur fracture model.BMC musculoskeletal disorders · 2026Article
- Upregulation of T-type voltage-dependent Ca²⁺ channels in activated hepatic stellate cells promotes liver fibrosis in metabolic dysfunction-associated steatohepatitis.Pflugers Archiv : European journal of physiology · 2026Article
- A natural small molecule alleviates liver fibrosis by targeting apolipoprotein L2.Nature chemical biology · 2025Article
- An L-type calcium channel blocker nimodipine exerts anti-fibrotic effects by attenuating TGF-β1 induced calcium response in an in vitro model of thyroid eye disease.Eye and vision (London, England) · 2024Article
- Article
- A Comprehensive Retrospective Study on the Mechanisms of Cyclic Mechanical Stretch-Induced Vascular Smooth Muscle Cell Death Underlying Aortic Dissection and Potential Therapeutics for Preventing Acute Aortic Aneurysm and Associated Ruptures.International journal of molecular sciences · 2024Review
- Calcium-Signalling in Human Glaucoma Lamina Cribrosa Myofibroblasts.International journal of molecular sciences · 2023Review
- Therapeutic Usefulness of a Novel Calcium Channel Blocker Azelnidipine in the Treatment of Hypertension: A Narrative Review.Cardiology and therapy · 2022Review
- Silencing of CD147 inhibits hepatic stellate cells activation related to suppressing aerobic glycolysis via hedgehog signaling.Cytotechnology · 2021Article
- AMPK-mTOR-ULK1-mediated autophagy protects carbon tetrachloride-induced acute hepatic failure by inhibiting p21 in rats.Journal of toxicologic pathology · 2021Article
- Nogo-C regulates post myocardial infarction fibrosis through the interaction with ER CaCell death & disease · 2018Article
- Dust particles-induced intracellular CaThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017Article
- Inhibition of Store-Operated Calcium Entry Protects Endothelial Progenitor Cells from H2O2-Induced Apoptosis.Biomolecules & therapeutics · 2016Article
- 1,4-Dihydropyridine Derivatives: Dihydronicotinamide Analogues-Model Compounds Targeting Oxidative Stress.Oxidative medicine and cellular longevity · 2016Review
- Mouse models of liver fibrosis mimic human liver fibrosis of different etiologies.Current pathobiology reports · 2014Article
- Antioxidant properties of proanthocyanidins attenuate carbon tetrachloride (CCl4)-induced steatosis and liver injury in rats via CYP2E1 regulation.Journal of medicinal food · 2014Article
- Azelnidipine inhibits cultured rat aortic smooth muscle cell death induced by cyclic mechanical stretch.PloS one · 2014Article
- Quercetin inhibits the cytotoxicity and oxidative stress in liver of rats fed aflatoxin-contaminated diet.Toxicology reports · 2014Article
- Article
- Azelnidipine prevents cardiac dysfunction in streptozotocin-diabetic rats by reducing intracellular calcium accumulation, oxidative stress and apoptosis.Cardiovascular diabetology · 2011Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeOxidative stress plays a critical role in liver fibrogenesis. Reactive oxygen species (ROS) stimulate hepatic stellate cells (HSCs), and ROS-mediated increases in calcium influx further increase ROS production. Azelnidipine is a calcium blocker that has been shown to have antioxidant effects in endothelial cells and cardiomyocytes. Therefore, we evaluated the anti-fibrotic and antioxidative effects of azelnidipine on liver fibrosis. EXPERIMENTAL APPROACH: We used TGF-β1-activated LX-2 cells (a human HSC line) and mouse models of fibrosis induced by treatment with either carbon tetrachloride (CCl(4) ) or thioacetamide (TAA). KEY
resultsAzelnidipine inhibited TGF-β1 and angiotensin II (Ang II)-activated α1(I) collagen mRNA expression in HSCs. Furthermore, TGF-β1- and Ang II-induced oxidative stress and TGF-β1-induced p38 and JNK phosphorylation were reduced in HSCs treated with azelnidipine. Azelnidipine significantly decreased inflammatory cell infiltration, pro-fibrotic gene expressions, HSC activation, lipid peroxidation, oxidative DNA damage and fibrosis in the livers of CCl(4) - or TAA-treated mice. Finally, azelnidipine prevented a decrease in the expression of some antioxidant enzymes and accelerated regression of liver fibrosis in CCl(4) -treated mice. CONCLUSIONS AND IMPLICATIONS: Azelnidipine inhibited TGF-β1- and Ang II-induced HSC activation in vitro and attenuated CCl(4) - and TAA-induced liver fibrosis, and it accelerated regression of CCl(4) -induced liver fibrosis in mice. The anti-fibrotic mechanism of azelnidipine against CCl(4) -induced liver fibrosis in mice may have been due an increased level of antioxidant defence. As azelnidipine is widely used in clinical practice without serious adverse effects, it may provide an effective new strategy for anti-fibrotic therapy.
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Registered trials
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