ArticleProceedings of the National Academy of Sciences of the United States of America2015
Neural activity and CaMKII protect mitochondria from fragmentation in aging Caenorhabditis elegans neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 68 citations in OpenAlex.
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- Mitochondrial Complex I and ROS control neuromuscular function through opposing pre- and postsynaptic mechanisms.PLoS biology · 2025Article
- Mitochondrial Complex I and ROS control neuromuscular function through opposing pre- and postsynaptic mechanisms.bioRxiv : the preprint server for biology · 2025Article
- Cigarette Tar Enhanced ECs Pyroptosis via CAMKII/Drp1/mtDNA: Novel Insight Into the Mechanism of Plaque Erosion.JACC. Basic to translational science · 2025Article
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- An Electrophysiological and Proteomic Analysis of the Effects of the Superoxide Dismutase Mimetic, MnTMPyP, on Synaptic Signalling Post-Ischemia in Isolated Rat Hippocampal Slices.Antioxidants (Basel, Switzerland) · 2023Article
- Exercise preserves physical fitness during aging through AMPK and mitochondrial dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- BAM15 Relieves Neurodegeneration in AgedMetabolites · 2022Article
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- Neuron-periphery mitochondrial stress communication in aging and diseases.Life medicine · 2022Review
- Oocyte mitophagy is critical for extended reproductive longevity.PLoS genetics · 2022Article
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- The Potential Implications of Hydrogen Sulfide in Aging and Age-Related Diseases through the Lens of Mitohormesis.Antioxidants (Basel, Switzerland) · 2022Review
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- Pleiotropic effects of mitochondria in aging.Nature aging · 2022Review
- Lack of age-related respiratory changes in Daphnia.Biogerontology · 2022Article
- The hypervariable region of atlastin-1 is a site for intrinsic and extrinsic regulation.The Journal of cell biology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Decline in mitochondrial morphology and function is a hallmark of neuronal aging. Here we report that progressive mitochondrial fragmentation is a common manifestation of aging Caenorhabditis elegans neurons and body wall muscles. We show that sensory-evoked activity was essential for maintaining neuronal mitochondrial morphology, and this activity-dependent mechanism required the Degenerin/ENaC sodium channel MEC-4, the L-type voltage-gated calcium channel EGL-19, and the Ca/calmodulin-dependent kinase II (CaMKII) UNC-43. Importantly, UNC-43 phosphorylated and inhibited the dynamin-related protein (DRP)-1, which was responsible for excessive mitochondrial fragmentation in neurons that lacked sensory-evoked activity. Moreover, enhanced activity in the aged neurons ameliorated mitochondrial fragmentation. These findings provide a detailed description of mitochondrial behavior in aging neurons and identify activity-dependent DRP-1 phosphorylation by CaMKII as a key mechanism in neuronal mitochondrial maintenance.
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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.