ArticleCell death & disease2018
Dysregulated autophagy contributes to caspase-dependent neuronal apoptosis.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 98 citations in OpenAlex.
- Investigation of the Effects of Saffron on Neuroprotection and Circadian Rhythm in anPharmaceuticals (Basel, Switzerland) · 2026Article
- Paeony root prevents 6-hydroxydopamine-induced neurotoxicity by regulating autophagic dysfunction via AKT signaling in Parkinson's disease models.Metabolic brain disease · 2025Article
- Neuronal Deletion ofBiomolecules · 2025Article
- Chrysin Modulates Behavior and Hippocampal Histopathology in Adult Male Hypoandrogenic Rats: The Regulatory Role of miR-30a, miR-375, and miR-204.Brain and behavior · 2025Article
- Conditional Overexpression of Neuritin in Supporting Cell Protects Cochlear Hair Cell and Delays Age-Related Hearing Loss by Enhancing Autophagy.International journal of molecular sciences · 2025Article
- Role of telomerase in the onset and treatment of gastric cancer.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- Ameliorating effect of S-Allyl cysteine (Black Garlic) on 6-OHDA mediated neurotoxicity in SH-SY5Y cell line.Toxicology reports · 2024Article
- Trehalose Attenuates In Vitro Neurotoxicity of 6-Hydroxydopamine by Reducing Oxidative Stress and Activation of MAPK/AMPK Signaling Pathways.International journal of molecular sciences · 2024Article
- Dietary restriction to optimize T cell immunity is an ancient survival strategy conserved in vertebrate evolution.Cellular and molecular life sciences : CMLS · 2023Article
- rt269L-Type hepatitis B virus (HBV) in genotype C infection leads to improved mitochondrial dynamics via the PERK-eIF2α-ATF4 axis in an HBx protein-dependent manner.Cellular & molecular biology letters · 2023Article
- Article
- New Insights of Early Brain Injury after Subarachnoid Hemorrhage: A Focus on the Caspase Family.Current neuropharmacology · 2023Article
- Dynamics of a model for the degradation mechanism of aggregated α-synuclein in Parkinson's disease.Frontiers in computational neuroscience · 2023Article
- Review
- Dysregulation of mitochondrial dynamics, mitophagy and apoptosis in major depressive disorder: Does inflammation play a role?Molecular psychiatry · 2022Article
- TGF-β1 Promotes Autophagy and Inhibits Apoptosis in Breast Cancer by Targeting TP63.Frontiers in oncology · 2022Article
- Lactoferrin Alleviated AFM1-Induced Apoptosis in Intestinal NCM 460 Cells through the Autophagy Pathway.Foods (Basel, Switzerland) · 2021Article
- FBXO7 triggers caspase 8-mediated proteolysis of the transcription factor FOXO4 and exacerbates neuronal cytotoxicity.The Journal of biological chemistry · 2021Article
- Omi inhibition ameliorates neuron apoptosis and neurological deficit after subarachnoid hemorrhage in rats.Genes & genomics · 2021Article
- Stellate Ganglion Block Improves the Proliferation and Function of Splenic CD4 + T Cells Through Inhibition of Posthemorrhagic Shock Mesenteric Lymph-Mediated Autophagy.Inflammation · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is a regulated, intracellular degradation process that delivers unnecessary or dysfunctional cargo to the lysosome. Autophagy has been viewed as an adaptive survival response to various stresses, whereas in other cases, it promotes cell death. Therefore, both deficient and excessive autophagy may lead to cell death. In this study, we specifically attempted to explore whether and how dysregulated autophagy contributes to caspase-dependent neuronal cell death induced by the neurotoxin 6-hydroxydopamine (6-OHDA). Ultrastructural and biochemical analyses indicated that MN9D neuronal cells and primary cultures of cortical neurons challenged with 6-OHDA displayed typical features of autophagy. Cotreatment with chloroquine and monitoring autophagic flux by a tandem mRFP-EGFP-tagged LC3 probe indicated that the autophagic phenomena were primarily caused by dysregulated autophagic flux. Consequently, cotreatment with an antioxidant but not with a pan-caspase inhibitor significantly blocked 6-OHDA-stimulated dysregulated autophagy. These results indicated that 6-OHDA-induced generation of reactive oxygen species (ROS) played a critical role in triggering neuronal death by causing dysregulated autophagy and subsequent caspase-dependent apoptosis. The results of the MTT reduction, caspase-3 activation, and TUNEL assays indicated that pharmacological inhibition of autophagy using 3-methyladenine or deletion of the autophagy-related gene Atg5 significantly inhibited 6-OHDA-induced cell death. Taken together, our results suggest that abnormal induction of autophagic flux promotes apoptotic neuronal cell death, and that the treatments limiting dysregulated autophagy may have a strong neuroprotective potential.
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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.