ArticleCNS neuroscience & therapeutics2016
Mitochondrial Membrane Potential-dependent Endoplasmic Reticulum Fragmentation is an Important Step in Neuritic Degeneration.
Article in CNS neuroscience & therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Parkinson's disease-associated PLA2G6 protects IP3R1 protein to control ER-mitochondria tethering and CaNature communications · 2026Article
- Glucose restriction induces degeneration of neurons with mitochondrial DNA depletion by altering ER-mitochondria calcium transfer.Molecular psychiatry · 2025Article
- Inhibition of SGLT2 protects podocytes in diabetic kidney disease by rebalancing mitochondria-associated endoplasmic reticulum membranes.Cell communication and signaling : CCS · 2024Article
- Suberoylanilide hydroxamic acid upregulates reticulophagy receptor expression and promotes cell death in hepatocellular carcinoma cells.World journal of gastroenterology · 2023Article
- Advances in Human Mitochondria-Based Therapies.International journal of molecular sciences · 2022Review
- Article
- Organelle remodeling in somatic cell reprogramming.Journal of molecular cell biology · 2020Review
- Alpha-Synuclein Toxicity on Protein Quality Control, Mitochondria and Endoplasmic Reticulum.Neurochemical research · 2018Review
- Polybrene induces neural degeneration by bidirectional CaCell death & disease · 2018Article
- Neurotropin® alleviates hippocampal neuron damage through a HIF-1α/MAPK pathway.CNS neuroscience & therapeutics · 2017Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuritic degeneration is an important early pathological step in neurodegeneration.
aimThe purpose of this study was to explore the mechanisms connecting neuritic degeneration to the functional and morphological remodeling of endoplasmic reticulum (ER) and mitochondria.
methodsHere, we set up neuritic degeneration models by neurite cutting-induced neural degeneration in human-induced pluripotent stem cell-derived neurons.
resultsWe found that neuritic ER becomes fragmented and forms complexes with mitochondria, which induces IP3R-dependent mitochondrial Ca(2+) elevation and dysfunction during neuritic degeneration. Furthermore, mitochondrial membrane potential is required for ER fragmentation and mitochondrial Ca(2+) elevation during neuritic degeneration. Mechanically, tightening of the ER-mitochondria associations by expression of a short "synthetic linker" and ER Ca(2+) releasing together could promote mitochondrial Ca(2+) elevation, dysfunction, and reactive oxygen species generation.
conclusionOur study reveals a dynamic remodeling of the ER-mitochondria interface underlying neuritic degeneration.
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