ArticleScientific reports2017
Homocysteine induces mitochondrial dysfunction involving the crosstalk between oxidative stress and mitochondrial pSTAT3 in rat ischemic brain.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 70 citations in OpenAlex.
- HBV re-activation is associated with increased mortality and dysregulation of oxidative and polyamine metabolism in pre-acute-on-chronic liver failure.Cell communication and signaling : CCS · 2026Article
- Betaine Attenuates Hyperhomocysteinemia-Induced Cognitive Impairment by Suppressing Oxidative Stress and Activating the PI3K/AKT/GSK-3β Pathway.Antioxidants (Basel, Switzerland) · 2026Article
- Modulation of mitochondrial dysfunction: Mechanisms and strategies for the use of natural products to treat stroke.Neural regeneration research · 2026Article
- SHMT2 deficiency disrupts transcriptional regulation through homocysteine-mediated suppression of histone lactylation in Huntington's disease models.The Journal of clinical investigation · 2026Article
- Homocysteine interferes with Ndufa1 leading to mitochondrial dysfunction through repression of the NADCell death & disease · 2025Article
- AIMP3 maintains cardiac homeostasis by regulating the editing activity of methionyl-tRNA synthetase.Nature cardiovascular research · 2025Article
- The involvement of the synaptic vesicle cycle in homocysteine induced neurotoxicity in vitro and in vivo.Scientific reports · 2025Article
- Neuroinflammation and Natural Antidepressants: Balancing Fire with Flora.Biomedicines · 2025Review
- Folate alleviated skin inflammation and fibrosis resulting from impaired homocysteine metabolism.Redox biology · 2025Article
- Mitochondrial dysfunction in Spaceflight Associated Neuro-Ocular Syndrome (SANS): a molecular hypothesis in pathogenesis.Eye (London, England) · 2024Article
- Gut Symptoms, Gut Dysbiosis and Gut-Derived Toxins in ALS.International journal of molecular sciences · 2024Review
- NMR based Serum metabolomics revealed metabolic signatures associated with oxidative stress and mitochondrial damage in brain stroke.Metabolic brain disease · 2024Article
- Homocysteine and mitochondrial quality control in diabetic retinopathy.Eye and vision (London, England) · 2024Article
- Higher homocysteine and fibrinogen are associated with early-onset post-stroke depression in patients with acute ischemic stroke.Frontiers in psychiatry · 2024Article
- Methylenetetrahydrofolate reductase polymorphisms in dental caries-induced pulp inflammation and regeneration of dentine-pulp complex: Future perspectives.The Saudi dental journal · 2023Article
- Prophylactic supplement with melatonin prevented the brain injury after cardiac arrest in rats.Scientific reports · 2023Article
- The Role of Methionine-Rich Diet in Unhealthy Cerebrovascular and Brain Aging: Mechanisms and Implications for Cognitive Impairment.Nutrients · 2023Review
- Lesion location and serum levels of homocysteine are associated with early-onset post-stroke depression in acute ischemic stroke.Brain and behavior · 2023Article
- Advances of HAntioxidants (Basel, Switzerland) · 2023Review
- Serum Homocysteine and Vascular Calcification: Advances in Mechanisms, Related Diseases, and Nutrition.Korean journal of family medicine · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homocysteine (Hcy) has been shown to have a neurotoxic effect on ischemic brain cells; however, the underlying mechanisms remain incompletely understood. Here, we examined whether Hcy treatment influences mitochondria injury, oxidative stress, and mitochondrial STAT3 (mitoStat3) expression in rat ischemic brain. Our results demonstrated that Hcy treatment aggravated the damage of mitochondrial ultrastructure in the brain cortex and the dentate gyrus region of the hippocampus after focal cerebral ischemia. An elevated Hcy level was also accompanied by the significant inhibition of mitochondrial complex I-III enzymatic activities in addition to an increase in cytochrome c release. 8-Hydroxy-2'-deoxyguanosine (8-OHdG) content and mitoStat3 protein phosphorylation level were increased in Hcy-treated animals, whereas AG490, a Jak2 inhibitor, inhibited mitoStat3 phosphorylation as well as 8-OHdG levels induced by Hcy. In vitro studies revealed that Hcy also markedly increased reactive oxygen species (ROS) and mitoStat3 levels. In addition, the inhibition of pSTAT3 reduced Hcy-mediated increase in ROS levels, whereas quenching ROS using the ROS inhibitor glutathione ethyl ester inhibited Hcy-mediated pSTAT3 overactivation in Neuro2a cells. These findings suggest that the development of therapies that interfere with the ROS/pSTAT3 pathway may be helpful for treating cerebral infarction-related diseases associated with Hcy.
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