ArticleNature aging2024
Converting cell death into senescence by PARP1 inhibition improves recovery from acute oxidative injury.
Article in Nature aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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.
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Who cites it
22 citing papers in PubMed.
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Loss of Erbin in tubular epithelial cells sensitizes mice to acute kidney injury and aggravates renal fibrosis.The EMBO journal · 2026Article
- Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.Journal of hematology & oncology · 2026Review
- CBX4 stabilizes NEUROD1 through SUMO-ubiquitin crosstalk to delay β-cell senescence.Nature communications · 2026Article
- Gut Microbiota-Isoallolithocholic Acid Crosstalk Promotes Calcium Oxalate Kidney Stone Formation via PARP1-Mediated Parthanatos.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Insights into the therapeutic strategies for aging and aging-associated diseases.Signal transduction and targeted therapy · 2026Review
- Article
- Ageing-Dependent Thyroid Hormone Receptor α Reduction Activates IP3R1-Meditated CaCell proliferation · 2026Article
- Dual Roles and Therapeutic Prospects of Proximal Tubular Epithelial Cell Senescence in Acute Kidney Injury.Biomolecules · 2026Review
- Systematic prioritization of potential therapeutic targets for glomerulonephritis using multi-omics Mendelian randomization.PLoS computational biology · 2026Article
- STING-ERO1 signaling exacerbates PARylation-mediated parthanatos in sepsis.Cell communication and signaling : CCS · 2026Article
- Bruceine E, a natural quassinoid from Brucea javanica, inhibits PARthanatos via targeting PARP1 in ischemic stroke.Frontiers in pharmacology · 2026Article
- Synergistic interplay between UV and urban particulate matter exposure induces melanocyte senescence and contributes to human skin aging.Scientific reports · 2025Article
- Visualizing the chronicle of multiple cell fates using a near-IR dual-RNA/DNA-targeting probe.Science advances · 2025Article
- A Signature of Senescence Based on An Analysis of Selected Markers in Primary Vascular Smooth Muscle Cells Cultured In Vitro and Derived from Atherosclerotic Plaque.Aging and disease · 2025Article
- Emerging role of mitochondrial calcium levels in cellular senescence and in switching cell fates.Nature aging · 2025Article
- A Novel "Three-in-One" Copper-Based Metal-Organic Framework Nanozyme Eradicates Colorectal Cancer and Overcomes Chemoresistance for Tumor Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Protective effects of ghrelin on pancreas in fructose diet and streptozotocin-induced diabetic rats.Journal of molecular histology · 2024Article
- Mechanism of minocycline activating Nrf2/Hmox1 pathway to prevent ferroptosis and alleviate acute compartment syndrome.Journal of orthopaedic surgery and research · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
Excessive amounts of reactive oxygen species (ROS) lead to macromolecular damage and high levels of cell death with consequent pathological sequelae. We hypothesized that switching cell death to a tissue regenerative state could potentially improve the short-term and long-term detrimental effects of ROS-associated acute tissue injury, although the mechanisms regulating oxidative stress-induced cell fate decisions and their manipulation for improving repair are poorly understood. Here, we show that cells exposed to high oxidative stress enter a poly (ADP-ribose) polymerase 1 (PARP1)-mediated regulated cell death, and that blocking PARP1 activation promotes conversion of cell death into senescence (CODIS). We demonstrate that this conversion depends on reducing mitochondrial Ca2
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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.