ArticleMediators of inflammation2022
Candesartan Reduces Neuronal Apoptosis Caused by Ischemic Stroke via Regulating the FFAR1/ITGA4 Pathway.
Article in Mediators of inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 14 citations in OpenAlex.
- Molecular mechanisms of programmed cell death and potential targeted pharmacotherapy in ischemic stroke (Review).International journal of molecular medicine · 2025Review
- Modular-Based Synergetic Mechanisms of Jasminoidin and Ursodeoxycholic Acid in Cerebral Ischemia Therapy.Biomedicines · 2025Article
- Scutellarin Alleviates Neuronal Apoptosis in Ischemic Stroke via Activation of the PI3K/AKT Signaling Pathway.International journal of molecular sciences · 2025Article
- The role of angiotensin II type 1 receptor pathway in cerebral ischemia‒reperfusion injury: Implications for the neuroprotective effect of ARBs.Neuroprotection (Chichester, England) · 2024Review
- Functional candesartan loaded lipid nanoparticles for the control of diabetes-associated stroke: In vitroInternational journal of pharmaceutics: X · 2024Article
- Effects of Angiotensin Receptor Blockers on Streptozotocin-Induced Diabetic Cataracts.Journal of clinical medicine · 2023Article
- Enpp1 deficiency caused chondrocyte apoptosis by inhibiting AMPK signaling pathway.Journal of orthopaedic surgery and research · 2023Article
- Mitochondrial dysfunctions induce PANoptosis and ferroptosis in cerebral ischemia/reperfusion injury: from pathology to therapeutic potential.Frontiers in cellular neuroscience · 2023Review
- Uncovering Candidate mRNAs, Signaling Pathways and Immune Cells in Atherosclerotic Plaque and Ischemic Stroke.International journal of general medicine · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Ischemic stroke (IS) is a general term for necrosis of brain tissue caused by stenosis, occlusion of arteries supplying blood to the brain (carotid artery and vertebral artery), and insufficient blood supply to the brain. Cerebral ischemia is the main kind of IS causing cell damage. However, the underlying mechanism still needs to be clarified further. In this study, it was demonstrated that FFAR1 was a hub gene in IS. The expression of FFAR1 was increased in PC12 cells with OGD/R treatment. FFAR1 deficiency inhibited cell viability and induced cell apoptosis, which was reversed by FFAR1 overexpression. Moreover, candesartan, as a compound targeting FFAR1, facilitated cell viability and reduced cell apoptosis. The expression of ITGA4 was also high in OGD/R-PC12 cells as FFAR1. Furthermore, FFAR1 deficiency retarded the increasing of cell viability and inhibition of cell apoptosis by downregulation of Bax and Cleaved Caspase-3 in OGD/R-PC12 cells with candesartan treatment. In conclusion, candesartan may regulate neuronal apoptosis through FFAR1/ITGA4 axis.
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