ArticleJCI insight2019
PARP1 inhibition alleviates injury in ARH3-deficient mice and human cells.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 48 citations in OpenAlex.
- NovelNeurology. Genetics · 2026Article
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- Identification of MRVI1-interacting proteins by biotin-based proximity labelling reveals NPM-ALK-dependent interaction dynamics.Journal of biochemistry · 2025Article
- Review
- Phenotypic Diversity in Stress-induced Childhood-Onset Neurodegeneration with Variable Ataxia and Seizures: Novel Associations with Parkinsonism, Icthyosis and Cataract.Cerebellum (London, England) · 2025Article
- Research progress of deubiquitinating enzymes in cerebral ischemia-reperfusion injury.Frontiers in aging neuroscience · 2025Review
- ADP-ribose hydrolases: biological functions and potential therapeutic targets.Expert reviews in molecular medicine · 2024Review
- Novel heterozygous variant ofHeliyon · 2024Article
- Expanding the Spectrum of Stress-Induced Childhood-Onset Neurodegeneration with Variable Ataxia and Seizures (CONDSIAS).Cerebellum (London, England) · 2024Article
- Regulation of β-cell death by ADP-ribosylhydrolase ARH3 via lipid signaling in insulitis.Cell communication and signaling : CCS · 2024Article
- Regulation of Biomolecular Condensates by Poly(ADP-ribose).Chemical reviews · 2023Review
- Bag3 Regulates Mitochondrial Function and the Inflammasome Through Canonical and Noncanonical Pathways in the Heart.JACC. Basic to translational science · 2023Article
- Regulated necrosis pathways: a potential target for ischemic stroke.Burns & trauma · 2023Review
- ARH Family of ADP-Ribose-Acceptor Hydrolases.Cells · 2022Review
- Poly(ADP-ribose) Polymerase 1 Mediates Rab5 Inactivation after DNA Damage.International journal of molecular sciences · 2022Article
- Poly(ADP-ribose) drives condensation of FUS via a transient interaction.Molecular cell · 2022Article
- The key players of parthanatos: opportunities for targeting multiple levels in the therapy of parthanatos-based pathogenesis.Cellular and molecular life sciences : CMLS · 2022Review
- Biological function, mediate cell death pathway and their potential regulated mechanisms for post-mortem muscle tenderization of PARP1: A review.Frontiers in nutrition · 2022Review
- BiallelicLife science alliance · 2021Article
- Why structure and chain length matter: on the biological significance underlying the structural heterogeneity of poly(ADP-ribose).Nucleic acids research · 2021Article
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Poly(ADP-ribosyl)ation refers to the covalent attachment of ADP-ribose to protein, generating branched, long chains of ADP-ribose moieties, known as poly(ADP-ribose) (PAR). Poly(ADP-ribose) polymerase 1 (PARP1) is the main polymerase and acceptor of PAR in response to DNA damage. Excessive intracellular PAR accumulation due to PARP1 activation leads cell death in a pathway known as parthanatos. PAR degradation is mainly controlled by poly(ADP-ribose) glycohydrolase (PARG) and ADP-ribose-acceptor hydrolase 3 (ARH3). Our previous results demonstrated that ARH3 confers protection against hydrogen peroxide (H2O2) exposure, by lowering cytosolic and nuclear PAR levels and preventing apoptosis-inducing factor (AIF) nuclear translocation. We identified a family with an ARH3 gene mutation that resulted in a truncated, inactive protein. The 8-year-old proband exhibited a progressive neurodegeneration phenotype. In addition, parthanatos was observed in neurons of the patient's deceased sibling, and an older sibling exhibited a mild behavioral phenotype. Consistent with the previous findings, the patient's fibroblasts and ARH3-deficient mice were more sensitive, respectively, to H2O2 stress and cerebral ischemia/reperfusion-induced PAR accumulation and cell death. Further, PARP1 inhibition alleviated cell death and injury resulting from oxidative stress and ischemia/reperfusion. PARP1 inhibitors may attenuate the progression of neurodegeneration in affected patients with ARH3 deficiency.
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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.