ArticleCell death & disease2018
Propofol inhibits parthanatos via ROS-ER-calcium-mitochondria signal pathway in vivo and vitro.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
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Who cites it
64 citing papers in PubMed, 104 citations in OpenAlex.
- Mitochondrial-endoplasmic reticulum interactions in lung diseases.Cell death & disease · 2026Review
- Gypenoside XLIX and Mitochondria-Associated ER Membranes in Non-Alcoholic Fatty Liver Disease: Mechanistic Insights and Emerging Perspectives.Molecules (Basel, Switzerland) · 2026Review
- Enhanced Antitumor Response in Breast Cancer via Parthanatos Activation Mediated by the Synergistic Effect of Etoposide and Resveratrol.Current issues in molecular biology · 2026Article
- Propofol regulates METTL3-mediated PARP-1 mScientific reports · 2026Article
- Regulated cell death in organ transplantation: recent developments and mechanistic overview.Journal of molecular cell biology · 2026Review
- Non-apoptotic Regulated Cell Death Mechanisms in Sepsis and their Therapeutic Potential.Inflammation · 2026Review
- Immaturity-Dependent Hippocampal Neurogenic Promotion and Fate Shift by Low-Dose Propofol in Neonatal Mice Revealed Through Single-Nuclei RNA-Sequencing.Biomedicines · 2025Article
- OAC1 improves mitofusin 2 expression to alleviate neuronal injury following experimental ischemic stroke.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Bidirectional Relationship Between Anaesthetic Drugs and Metabolic Syndrome: Clinical Effects and Mechanisms.Journal of cellular and molecular medicine · 2025Review
- Silica Nanoparticles Induce SH-SY5Y Cells Death Via PARP and Caspase Signaling Pathways.Molecular neurobiology · 2025Article
- Anesthetics in pathological cerebrovascular conditions.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Review
- Phillygenin ameliorates tight junction proteins reduction, fibrosis, and apoptosis in mice with chronic colitis via TGR5-mediated PERK-eIF2α-CaJournal of pharmaceutical analysis · 2025Article
- Advances in research on propofol-induced postoperative cognitive dysfunction via Piezo channels.Frontiers in molecular neuroscience · 2025Review
- Exercise training alleviates neuronal apoptosis and re-establishes mitochondrial quality control after cerebral ischemia by increasing SIRT3 expression.Cell biology and toxicology · 2024Article
- Newcastle disease virus infection induces parthanatos in tumor cells via calcium waves.PLoS pathogens · 2024Article
- Ginsenoside Rg1: A Neuroprotective Natural Dammarane-Type Triterpenoid Saponin With Anti-Depressive Properties.CNS neuroscience & therapeutics · 2024Review
- Suppression of JNK pathway protects neurons from oxidative injury via attenuating parthanatos in glutamate-treated HT22 neurons.Scientific reports · 2024Article
- Ozone therapy mitigates parthanatos after ischemic stroke.Biological research · 2024Article
- Exploring Research Trend and Hotspots on Oxidative Stress in Ischemic Stroke (2001-2022): Insights from Bibliometric.Molecular neurobiology · 2024Review
- Parthanatos initiated by ROS-induced DNA damage is involved in intestinal epithelial injury during necrotizing enterocolitis.Cell death discovery · 2024Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parthanatos is a new form of programmed cell death. It has been recognized to be critical in cerebral ischemia-reperfusion injury, and reactive oxygen species (ROS) can induce parthanatos. Recent studies found that propofol, a widely used intravenous anesthetic agent, has an inhibitory effect on ROS and has neuroprotective in many neurological diseases. However, the functional roles and mechanisms of propofol in parthanatos remain unclear. Here, we discovered that the ROS-ER-calcium-mitochondria signal pathway mediated parthanatos and the significance of propofol in parthanatos. Next, we found that ROS overproduction would cause endoplasmic reticulum (ER) calcium release, leading to mitochondria depolarization with the loss of mitochondrial membrane potential. Mitochondria depolarization caused mitochondria to release more ROS, which, in turn, contributed to parthanatos. Also, we found that propofol inhibited parthanatos through impeding ROS overproduction, calcium release from ER, and mitochondrial depolarization in parthanatos. Importantly, our results indicated that propofol protected cerebral ischemia-reperfusion via parthanatos suppression, amelioration of mitochondria, and ER swelling. Our findings provide new insights into the mechanisms of how ER and mitochondria contribute to parthanatos. Furthermore, our studies elucidated that propofol has a vital role in parthanatos prevention in vivo and in vitro, and propofol can be a promising therapeutic approach for nerve injury patients.
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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.