ReviewMolecular neurobiology2010
Poly(ADP-ribose) metabolism in brain and its role in ischemia pathology.
Review in Molecular neurobiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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
34 citing papers in PubMed, 55 citations in OpenAlex.
- PJ34 Prevents Trauma-Induced Heterotopic Ossification without Adverse Bone Healing: An in vivo and in vitro Investigation.Drug design, development and therapy · 2026Article
- Gastrodin: a potential natural product for the prevention and treatment of cerebral ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- Modulation of Excitatory Synaptic Transmission During Cannabinoid Receptor Activation.Cellular and molecular neurobiology · 2022Article
- Poly (ADP-ribose) polymerase: An Overview of Mechanistic Approaches and Therapeutic Opportunities in the Management of Stroke.Neurochemical research · 2022Review
- Article
- Emerging neuroprotective strategies for the treatment of ischemic stroke: An overview of clinical and preclinical studies.Experimental neurology · 2021Review
- Article
- The Modified Phenanthridine PJ34 Unveils an Exclusive Cell-Death Mechanism in Human Cancer Cells.Cancers · 2020Review
- The Novel Role of PPAR Alpha in the Brain: Promising Target in Therapy of Alzheimer's Disease and Other Neurodegenerative Disorders.Neurochemical research · 2020Review
- Antiapoptotic and Anti-Inflammatory Effects of CPCGI in Rats with Traumatic Brain Injury.Neuropsychiatric disease and treatment · 2020Article
- Multi-targeted Effect of Nicotinamide Mononucleotide on Brain Bioenergetic Metabolism.Neurochemical research · 2019Review
- Interplay between NADBiochimica et biophysica acta. Molecular basis of disease · 2019Review
- HX600, a synthetic agonist for RXR-Nurr1 heterodimer complex, prevents ischemia-induced neuronal damage.Brain, behavior, and immunity · 2018Article
- Early Treatment with Poly(ADP-Ribose) Polymerase-1 Inhibitor (JPI-289) Reduces Infarct Volume and Improves Long-Term Behavior in an Animal Model of Ischemic Stroke.Molecular neurobiology · 2018Article
- Inhibition of Poly(ADP-ribose) Polymerase-1 Enhances Gene Expression of Selected Sirtuins and APP Cleaving Enzymes in Amyloid Beta Cytotoxicity.Molecular neurobiology · 2018Article
- Opportunities for the repurposing of PARP inhibitors for the therapy of non-oncological diseases.British journal of pharmacology · 2018Review
- Alpha-synuclein alters differently gene expression of Sirts, PARPs and other stress response proteins: implications for neurodegenerative disorders.Molecular neurobiology · 2018Article
- Effects of Poly(ADP-Ribose) Polymerase-1 Inhibition in a Neonatal Rodent Model of Hypoxic-Ischemic Injury.BioMed research international · 2017Article
- Inferring Molecular Processes Heterogeneity from Transcriptional Data.BioMed research international · 2017Article
- Gastrodin ameliorates subacute phase cerebral ischemia‑reperfusion injury by inhibiting inflammation and apoptosis in rats.Molecular medicine reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The biological roles of poly(ADP-ribose) polymers (PAR) and poly(ADP-ribosyl)ation of proteins in the central nervous system are diverse. The homeostasis of PAR orchestrated by poly(ADP-ribose) polymerase-1 (PARP-1) and poly(ADP-ribose) glycohydrolase (PARG) is crucial for cell physiology and pathology. Both enzymes are ubiquitously distributed in neurons and glia; however, they are segregated at the subcellular level. PARP-1 serves as a "nick sensor" for single- or double-stranded breaks in DNA and is involved in long and short patch base-excision repair, while PARG breaks down PAR. The stimulation of PARP-1 and PAR formation can activate proinflammatory transcription factors, including nuclear factor kappa B. However, hyperactivation of PARP-1 can result in depletion of NAD/ATP, and in PAR-dependent mitochondrial pore formation leading to release of apoptosis inducing factor and cell death. The role of PAR as a death signaling molecule in brain ischemia-reperfusion and inflammation as well as the effect of gender and aging is presented in this review. Modulating the PAR level through pharmacological or genetic intervention on PARP-1/PARG activity and gene expression should be a valuable way for neuroprotective strategy.
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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.