ReviewTranslational stroke research2014
Mitochondrial dysfunction induced by nuclear poly(ADP-ribose) polymerase-1: a treatable cause of cell death in stroke.
Review in Translational stroke research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 66 citations in OpenAlex.
- Selective targeting of genome amplifications and repeat elements by CRISPR-Cas9 nickases to promote cancer cell death.Nature communications · 2025Article
- Exploring the role of parthanatos in CNS injury: Molecular insights and therapeutic approaches.Journal of advanced research · 2025Review
- The Untargeted Metabolomics Reveals Differences in Energy Metabolism in Patients with Different Subtypes of Ischemic Stroke.Molecular neurobiology · 2024Article
- Role of NADCellular and molecular neurobiology · 2023Review
- DNA damage response signaling: A common link between cancer and cardiovascular diseases.Cancer medicine · 2023Review
- Poly (ADP-ribose) polymerase: An Overview of Mechanistic Approaches and Therapeutic Opportunities in the Management of Stroke.Neurochemical research · 2022Review
- Review
- Endoplasmic Reticulum Interaction Supports Energy Production and Redox Homeostasis in Mitochondria Released from Astrocytes.Translational stroke research · 2021Article
- Cytostatic Effect of a Novel Mitochondria-Targeted Pyrroline Nitroxide in Human Breast Cancer Lines.International journal of molecular sciences · 2021Article
- DNase II mediates a parthanatos-like developmental cell death pathway in Drosophila primordial germ cells.Nature communications · 2021Article
- Role of Oxidative DNA Damage and Repair in Atrial Fibrillation and Ischemic Heart Disease.International journal of molecular sciences · 2021Review
- Involvement of Mitochondrial Mechanisms in the Cytostatic Effect of Desethylamiodarone in B16F10 Melanoma Cells.International journal of molecular sciences · 2020Article
- Mitochondrial Protection by PARP Inhibition.International journal of molecular sciences · 2020Review
- Mitochondrial protective effect of neferine through the modulation of nuclear factor erythroid 2-related factor 2 signalling in ischaemic stroke.British journal of pharmacology · 2019Article
- ADP-ribosylation: from molecular mechanisms to human disease.Genetics and molecular biology · 2019Article
- NLRP3 Inflammasome in the Pathophysiology of Hemorrhagic Stroke: A Review.Current neuropharmacology · 2019Review
- Electroacupuncture Inhibits Apoptosis of Peri-Ischemic Regions via Modulating p38, Extracellular Signal-Regulated Kinase (ERK1/2), and c-Jun N Terminal Kinases (JNK) in Cerebral Ischemia-Reperfusion-Injured Rats.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- The NADAntioxidants & redox signaling · 2018Review
- P2X7 Receptor-Associated Programmed Cell Death in the Pathophysiology of Hemorrhagic Stroke.Current neuropharmacology · 2018Review
- Opportunities for the repurposing of PARP inhibitors for the therapy of non-oncological diseases.British journal of pharmacology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Many drugs targeting excitotoxic cell death have demonstrated robust neuroprotective effects in animal models of cerebral ischemia. However, these neuroprotective effects have almost universally required drug administration at relatively short time intervals after ischemia onset. This finding has translated to clinical trial results; interventions targeting excitotoxicity have had no demonstrable efficacy when initiated hours after ischemia onset, but beneficial effects have been reported with more rapid initiation. Consequently, there continues to be a need for interventions with efficacy at later time points after ischemia. Here, we focus on mitochondrial dysfunction as both a relatively late event in ischemic neuronal death and a recognized cause of delayed neuronal death. Activation of poly(ADP-ribose) polymerase-1 (PARP-1) is a primary cause of mitochondrial depolarization and subsequent mitochondria-triggered cell death in ischemia reperfusion. PARP-1 consumes cytosolic NAD(+), thereby blocking both glycolytic ATP production and delivery of glucose carbon to mitochondria for oxidative metabolism. However, ketone bodies such as pyruvate, beta- and gamma-hydroxybutyrate, and 1,4-butanediol can fuel mitochondrial metabolism in cells with depleted cytosolic NAD(+) as long as the mitochondria remain functional. Ketone bodies have repeatedly been shown to be highly effective in preventing cell death in animal models of ischemia, but a rigorous study of the time window of opportunity for this approach remains to be performed.
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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.