ArticleMolecules and cells2013
Induction of mitochondrial dysfunction by poly(ADP-ribose) polymer: implication for neuronal cell death.
Article in Molecules and cells, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 31 citations in OpenAlex.
- HM568 Enhances NADMolecular neurobiology · 2026Article
- Novel clinical potential of poly (ADP‑ribose) polymerase inhibitors in triple‑negative breast cancer: Mechanistic insights and clinical applications (Review).Oncology letters · 2025Review
- Nicotinamide mononucleotide combined with PJ-34 protects microglial cells from lipopolysaccharide-induced mitochondrial impairment through NMNAT3-PARP1 axis.Journal of translational medicine · 2025Article
- Zinc defends against Parthanatos and promotes functional recovery after spinal cord injury through SIRT3-mediated anti-oxidative stress and mitophagy.CNS neuroscience & therapeutics · 2023Article
- Pathomechanisms of Inherited Retinal Degeneration and Perspectives for Neuroprotection.Cold Spring Harbor perspectives in medicine · 2023Review
- Regulated cell death (RCD) in cancer: key pathways and targeted therapies.Signal transduction and targeted therapy · 2022Review
- NUPR1 protects against hyperPARylation-dependent cell death.Communications biology · 2022Article
- Inherited Retinal Degeneration: PARP-Dependent Activation of Calpain Requires CNG Channel Activity.Biomolecules · 2022Article
- The DNA-damage response and nuclear events as regulators of nonapoptotic forms of cell death.Oncogene · 2020Review
- Caspase-Independent Regulated Necrosis Pathways as Potential Targets in Cancer Management.Frontiers in oncology · 2020Review
- SIRT3 Regulation Under Cellular Stress: Making Sense of the Ups and Downs.Frontiers in neuroscience · 2018Article
- Upregulation of Spinal Voltage-Dependent Anion Channel 1 Contributes to Bone Cancer Pain Hypersensitivity in Rats.Neuroscience bulletin · 2017Article
- Deficiency of Parkinson's disease-related gene Fbxo7 is associated with impaired mitochondrial metabolism by PARP activation.Cell death and differentiation · 2017Article
- Mitochondrial poly(ADP-ribose) polymerase: The Wizard of Oz at work.Free radical biology & medicine · 2016Review
- FAF1 mediates regulated necrosis through PARP1 activation upon oxidative stress leading to dopaminergic neurodegeneration.Cell death and differentiation · 2016Article
- Inhibition of prostaglandin E2 receptor EP3 mitigates thrombin-induced brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
- Permeability transition pore-dependent and PARP-mediated depletion of neuronal pyridine nucleotides during anoxia and glucose deprivation.Journal of bioenergetics and biomembranes · 2015Article
- Sex differences in mitochondrial (dys)function: Implications for neuroprotection.Journal of bioenergetics and biomembranes · 2015Review
- Melatonin and Ischemic Stroke: Mechanistic Roles and Action.Advances in pharmacological sciences · 2015Review
- Modulation of mitochondrial function and autophagy mediates carnosine neuroprotection against ischemic brain damage.Stroke · 2014Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poly(ADP-ribose) polymerase-1 (PARP-1) mediates neuronal cell death in a variety of pathological conditions involving severe DNA damage. Poly(ADP-ribose) (PAR) polymer is a product synthesized by PARP-1. Previous studies suggest that PAR polymer heralds mitochondrial apoptosis-inducing factor (AIF) release and thereby, signals neuronal cell death. However, the details of the effects of PAR polymer on mitochondria remain to be elucidated. Here we report the effects of PAR polymer on mitochondria in cells in situ and isolated brain mitochondria in vitro. We found that PAR polymer causes depolarization of mitochondrial membrane potential and opening of the mitochondrial permeability transition pore early after injury. Furthermore, PAR polymer specifically induces AIF release, but not cytochrome c from isolated brain mitochondria. These data suggest PAR polymer as an endogenous mitochondrial toxin and will further our understanding of the PARP-1-dependent neuronal cell death paradigm.
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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.