ArticleMolecular neurobiology2019
Inhibition of Autophagy by Captopril Attenuates Prion Peptide-Mediated Neuronal Apoptosis via AMPK Activation.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 35 citations in OpenAlex.
- Calcium-dependent serine-threonine phosphatase and autophagy inactivation mediated by Baicalein attenuates prion protein-mediated neuronal cell damage.BMC complementary medicine and therapies · 2025Article
- High risk factors, molecular features and clinical management for radioactive iodine-refractory differentiated thyroid carcinoma.Frontiers in oncology · 2025Review
- Melatonin-mediated calcineurin inactivation attenuates amyloid beta-induced apoptosis.IBRO neuroscience reports · 2024Article
- The scheme, and regulative mechanism of pyroptosis, ferroptosis, and necroptosis in radiation injury.International journal of biological sciences · 2024Review
- Melatonin inhibits Japanese encephalitis virus replication and neurotoxicity via calcineurin-autophagy pathways.BMC neuroscience · 2023Article
- Endothelial Sp1/Sp3 are essential to the effect of captopril on blood pressure in male mice.Nature communications · 2023Article
- Thymosin Beta 4 Protects Hippocampal Neuronal Cells against PrP (106-126) via Neurotrophic Factor Signaling.Molecules (Basel, Switzerland) · 2023Article
- Impact of the Renin-Angiotensin System on the Pathogeny and Pharmacotherapeutics of Neurodegenerative Diseases.Biomolecules · 2022Review
- Moxibustion alleviates chronic heart failure by regulating mitochondrial dynamics and inhibiting autophagy.Experimental and therapeutic medicine · 2022Article
- Captopril exhibits protective effects through anti-inflammatory and anti-apoptotic pathways against hydrogen peroxide-induced oxidative stress in C6 glioma cells.Metabolic brain disease · 2022Article
- EZH2 targeting to improve the sensitivity of acquired radio-resistance bladder cancer cells.Translational oncology · 2022Article
- The interplay between oxidative stress and autophagy: focus on the development of neurological diseases.Behavioral and brain functions : BBF · 2022Review
- Pyrroloquinoline quinone promotes mitochondrial biogenesis in rotenone-induced Parkinson's disease model via AMPK activation.Acta pharmacologica Sinica · 2021Article
- Calcineurin Activation by Prion Protein Induces Neurotoxicity via Mitochondrial Reactive Oxygen Species.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of prion protein (PrPc) into a protease-resistant form (PrPsc) in the brains of humans and animals affects the central nervous system. PrPsc occurs only in mammals with transmissible prion diseases. Prion protein refers to either the infectious pathogen itself or the main component of the pathogen. Recent studies suggest that autophagy is one of the major functions that keep cells alive and which has a protective effect against neurodegeneration. In this study, we investigated whether the anti-hypertensive drug, captopril, could attenuate prion peptide PrP (106-126)-induced calcium alteration-mediated neurotoxicity. Treatment with captopril increased both LC3-II (microtubule-associated protein 1A/1B-light chain 3-II) and p62 protein levels, indicating autophagy flux inhibition. Electron microscopy confirmed the occurrence of autophagic flux inhibition in neuronal cells treated with captopril. Captopril attenuated PrP (106-126)-induced neuronal cell death via AMPK activation and autophagy inhibition. Compound C suppressed AMPK activation as well as the neuroprotective effects of captopril. Thus, these data showed that an anti-hypertensive drug has a protective effect against prion-mediated neuronal cell death via autophagy inhibition and AMPK activation, and also suggest that anti-hypertensive drugs may be effective therapeutic agents against neurodegenerative disorders, including prion diseases.
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