ArticleFrontiers in aging neuroscience2015
Miro1 deficiency in amyotrophic lateral sclerosis.
Article in Frontiers in aging neuroscience, 2015. 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, 64 citations in OpenAlex.
- Mitochondrial Dysfunction: From Molecular Mechanisms to Modern Approaches for Basic and Clinical Research.Biomedicines · 2026Review
- Dual regulation of PINK1/PARKIN-mediated mitochondrial autophagy in ovarian cancer progression and drug resistance: mechanisms and therapeutic potentials.Journal of ovarian research · 2026Review
- Anxiety-Associated Behaviors Following Ablation ofeNeuro · 2026Article
- Synaptic-mitochondrial transport: mechanisms in neural adaptation and degeneration.Molecular and cellular biochemistry · 2025Review
- Expression Pattern of the AB1-Gal4 Driver inInternational journal of molecular sciences · 2025Article
- Mitochondria Dysfunction and Neuroinflammation in Neurodegeneration: Who Comes First?Antioxidants (Basel, Switzerland) · 2024Review
- Reversing Dysdynamism to Interrupt Mitochondrial Degeneration in Amyotrophic Lateral Sclerosis.Cells · 2023Review
- Miro GTPase domains regulate the assembly of the mitochondrial motor-adaptor complex.Life science alliance · 2023Article
- Role of Mitophagy in neurodegenerative Diseases and potential tagarts for Therapy.Molecular biology reports · 2022Review
- The compartmentalised nature of neuronal mitophagy: molecular insights and implications.Expert reviews in molecular medicine · 2022Review
- Protein lifetimes in aged brains reveal a proteostatic adaptation linking physiological aging to neurodegeneration.Science advances · 2022Article
- Broad activation of the Parkin pathway induces synaptic mitochondrial deficits in early tauopathy.Brain : a journal of neurology · 2022Article
- Effects of the Edaravone, a Drug Approved for the Treatment of Amyotrophic Lateral Sclerosis, on Mitochondrial Function and Neuroprotection.Antioxidants (Basel, Switzerland) · 2022Review
- Mitochondrial dynamics involves molecular and mechanical events in motility, fusion and fission.Frontiers in cell and developmental biology · 2022Review
- A Nanobody-Based Toolset to Monitor and Modify the Mitochondrial GTPase Miro1.Frontiers in molecular biosciences · 2022Article
- Miro1 Regulates Neuronal Mitochondrial Transport and Distribution to Alleviate Neuronal Damage in Secondary Brain Injury After Intracerebral Hemorrhage in Rats.Cellular and molecular neurobiology · 2021Article
- TRAK1-Mediated Abnormality of Mitochondrial Fission Increases Seizure Susceptibility in Temporal Lobe Epilepsy.Molecular neurobiology · 2021Article
- Sexual differences in mitochondrial and related proteins in rat cerebral microvessels: A proteomic approach.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Article
- The multifaceted role of kinases in amyotrophic lateral sclerosis: genetic, pathological and therapeutic implications.Brain : a journal of neurology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Proper transportation of mitochondria to sites with high energy demands is critical for neuronal function and survival. Impaired mitochondrial movement has been repeatedly reported in motor neurons of amyotrophic lateral sclerosis (ALS) patients and indicated as an important mechanism contributing to motor neuron degeneration in ALS. Miro1, a RhoGTPase also referred to as Rhot1, is a key regulator of mitochondrial movement linking mitochondria and motor proteins. In this study, we investigated whether the expression of Miro1 was altered in ALS patients and ALS animal models. Immunoblot analysis revealed that Miro1 was significantly reduced in the spinal cord tissue of ALS patients. Consistently, the decreased expression of Miro1 was also noted only in the spinal cord, and not in the brain tissue of transgenic mice expressing ALS-associated SOD1 G93A or TDP-43 M337V. Glutamate excitotoxicity is one of the major pathophysiological mechanisms implicated in the pathogenesis of ALS, and we found that excessive glutamate challenge lead to significant reduction of Miro1 expression in spinal cord motor neurons both in vitro and in mice. Taken together, these findings show Miro1 deficiency in ALS patients and ALS animal models and suggest glutamate excitotoxicity as a likely cause of Miro1 deficiency.
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Registered trials
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.