ArticleMolecular neurobiology2015
Role of Mitochondrial Calcium Uniporter in Early Brain Injury After Experimental Subarachnoid Hemorrhage.
Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Iron-driven secondary injury after intracranial hemorrhage: mitochondrial dysfunction and ferroptosis.Frontiers in neuroscience · 2026Review
- Article
- Mitochondrial stress: a key role of neuroinflammation in stroke.Journal of neuroinflammation · 2024Review
- Causal relationship between mitochondrial-associated proteins and cerebral aneurysms: a Mendelian randomization study.Frontiers in neurology · 2024Article
- Connection between oxidative stress and subcellular organelle in subarachnoid hemorrhage: Novel mechanisms and therapeutic implications.CNS neuroscience & therapeutics · 2023Review
- Human umbilical cord mesenchymal stem cell-derived exosome suppresses programmed cell death in traumatic brain injury via PINK1/Parkin-mediated mitophagy.CNS neuroscience & therapeutics · 2023Article
- Neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the Nrf2/ARE pathway.Brain and behavior · 2022Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- New Mechanisms and Targets of Subarachnoid Hemorrhage: A Focus on Mitochondria.Current neuropharmacology · 2022Review
- Ifenprodil Improves Long-Term Neurologic Deficits Through Antagonizing Glutamate-Induced Excitotoxicity After Experimental Subarachnoid Hemorrhage.Translational stroke research · 2021Article
- An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage.Frontiers in aging neuroscience · 2021Review
- Ferroptosis: New Dawn for Overcoming the Cardio-Cerebrovascular Diseases.Frontiers in cell and developmental biology · 2021Review
- Neuroprotective Effect of Oridonin on Traumatic Brain Injury via Inhibiting NLRP3 Inflammasome in Experimental Mice.Frontiers in neuroscience · 2020Article
- Modulation of Ion Transport Across Plant Membranes by Polyamines: Understanding Specific Modes of Action Under Stress.Frontiers in plant science · 2020Article
- Mitochondrial calcium uniporter regulates PGC-1α expression to mediate metabolic reprogramming in pulmonary fibrosis.Redox biology · 2019Article
- Role of mitochondrial calcium uniporter-mediated CaJournal of cellular and molecular medicine · 2019Article
- Iron regulatory protein deficiency compromises mitochondrial function in murine embryonic fibroblasts.Scientific reports · 2018Article
- TGF-β1 Regulation of P-JNK and L-Type Calcium Channel Cav1.2 in Cortical Neurons.Journal of molecular neuroscience : MN · 2018Article
- Inhibition of myeloid differentiation primary response protein 88 provides neuroprotection in early brain injury following experimental subarachnoid hemorrhage.Scientific reports · 2017Article
- Pterostilbene Attenuates Early Brain Injury Following Subarachnoid Hemorrhage via Inhibition of the NLRP3 Inflammasome and Nox2-Related Oxidative Stress.Molecular neurobiology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that mitochondrial Ca(2+) is undertaken by mitochondrial calcium uniporter (MCU), and its accumulation is associated with the development of many diseases. However, little was known about the role of MCU in early brain injury (EBI) after subarachnoid hemorrhage (SAH). MCU can be opened by spermine under a physiological condition and inhibited by ruthenium red (RR). Herein, we investigated the effects of RR and spermine to reveal the role of MCU in SAH animal model. The data obtained with biochemical and histological assays showed that mitochondrial Ca(2+) concentration was significantly increased in the temporal cortex of rats 1, 2, and 3 days after SAH, consistent with constant high levels of cellular Ca(2+) concentration. In agreement with the observation in the acute phase, SAH rats showed an obvious increase of reactive oxygen species (ROS) level and decrease of ATP production. Blockage of MCU prevented Ca(2+) accumulation, abated the level of oxidative stress, and improved the energy supply. Translocation of cytochrome c, increased cleaved caspase-3, and a large amount of apoptotic cells after SAH were reversed by RR administration. Surprisingly, exogenous spermine did not increase cellular Ca(2+) concentration, but lessened the Ca(2+) accumulation after SAH to benefit the rats. Taken together, our results demonstrated that blockage of MCU or prevention of Ca(2+) accumulation after SAH is essential in EBI after SAH. These findings suggest that MCU is considered to be a therapeutic target for patients suffering from SAH.
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