ArticleAnnals of translational medicine2022
The propofol-induced mitochondrial damage in fetal rat hippocampal neurons via the AMPK/P53 signaling pathway.
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Propofol regulates SLC6A2 expression via NAT10-mediated ac4C modification to modulate excessive mitophagy and hippocampal neuron dysfunction in aged postoperative cognitive dysfunction.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Propofol-Induced Mitochondrial Dysfunction Is Independent of Mitochondrial Permeability Transition.Biomedicines · 2025Article
- Astaxanthin Alleviates Oxidative Stress in Mouse Preantral Follicles and Enhances Follicular Development Through the AMPK Signaling Pathway.International journal of molecular sciences · 2025Article
- Induction of M1 polarization in BV2 cells by propofol intervention promotes perioperative neurocognitive disorders through the NGF/CREB signaling pathway: an experimental research.International journal of surgery (London, England) · 2025Article
- Exploring the correlation between Drp1 protein and the neurotoxicity of propofol.Frontiers in neuroscience · 2025Review
- The effects of general anesthetics on mitochondrial structure and function in the developing brain.Frontiers in neurology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Propofol is a commonly used general anesthetic that may cause neuronal damage, especially in infants and young children. Mitochondria play an essential role in cellular metabolism and signal transduction. Propofol may cause neurotoxicity by inhibiting mitochondrial function, but the mechanism by this which occurs remains unclear. Methods: First, the primary rat hippocampal neurons were cultured for 7 days Results: Higher propofol concentrations or longer incubation times were associated with more pronounced decreases in ATP, B-cell lymphoma 2 (Bcl-2), and mitochondrial membrane potential, and more pronounced increases in ROS, BCL2-associated X (Bax), Cytochrome C (CytC), and cleaved caspase-9. Additionally, after incubation with propofol (100 µM), neuronal Bcl-2, p-AMPK, ATP, and mitochondrial membrane potential were downregulated, and ROS, p53, CytC, Bax, cleaved caspase-3, and cleaved caspase-9 were upregulated. AMPK activators or p53 inhibitors reversed the above-mentioned changes. Conclusions: Propofol (100 µM)-induced mitochondrial damage in fetal rat hippocampal neurons may be mediated by the AMPK/p53 signaling pathway. Propofol (100 µM) was shown to inhibit the activity of AMPK in neurons, upregulate the expression of p53, and then activate the mitochondrial-dependent apoptosis pathway, which may lead to neuronal apoptosis.
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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.