ReviewFly2017
The beneficial role of extracellular reactive oxygen species in apoptosis-induced compensatory proliferation.
Review in Fly, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 35 citations in OpenAlex.
- Pharmacological Effects of NADPH Oxidase Inhibitors on Butterfly Wing Morphogenesis and Color Pattern Formation inInsects · 2026Article
- Single-cell RNA analysis reveals unexpected hemocyte plasticity and immune cell specialization in abioRxiv : the preprint server for biology · 2026Article
- Ythdc1-p300-Klf5 Complex-Mediated Golgi Dysfunction Promotes Aortic Aneurysm.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A threshold level of JNK activates damage-responsive enhancers via JAK/STAT to promote tissue regeneration.Development (Cambridge, England) · 2025Article
- Messages from Beyond the Grave: How Can Drosophila Help Us Understand the Consequences of Apoptosis?Advances in experimental medicine and biology · 2025Review
- The molecular mechanisms underlying the regeneration process in the earthworm, Perionyx excavatus exhibit indications of apoptosis-induced compensatory proliferation (AICP).In vitro cellular & developmental biology. Animal · 2024Article
- A culture model to analyze the acute biomaterial-dependent reaction of human primary neutrophilsBioactive materials · 2023Article
- Chitinase-like proteins promoting tumorigenesis through disruption of cell polarityFrontiers in oncology · 2023Article
- Mitochondrial DNA Repair in Neurodegenerative Diseases and Ageing.International journal of molecular sciences · 2022Review
- Integrin-ECM interactions and membrane-associated Catalase cooperate to promote resilience of the Drosophila intestinal epithelium.PLoS biology · 2022Article
- Progress in Vocal Fold Regenerative Biomaterials: An Immunological Perspective.Advanced nanobiomed research · 2022Article
- An Open Question: Is Non-Ionizing Radiation a Tool for Controlling Apoptosis-Induced Proliferation?International journal of molecular sciences · 2021Review
- Heat-KilledMolecules (Basel, Switzerland) · 2020Article
- Basement membrane damage by ROS- and JNK-mediated Mmp2 activation drives macrophage recruitment to overgrown tissue.Nature communications · 2020Article
- Dexmedetomidine alleviated neuropathic pain in dorsal root ganglion neurons by inhibition of anaerobic glycolysis activity and enhancement of ROS tolerance.Bioscience reports · 2020Article
- Epimedium Polysaccharide Ameliorates Benzene-Induced Aplastic Anemia in Mice.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- The significant impact of apigenin on different aspects of autoimmune disease.Inflammopharmacology · 2018Review
- Hydrogen Peroxide and Redox Regulation of Developments.Antioxidants (Basel, Switzerland) · 2018Review
- Variation in Mitochondria-Derived Transcript Levels Associated With DDT Resistance in the 91-R Strain of Drosophila melanogaster (Diptera: Drosophilidae).Journal of insect science (Online) · 2018Article
- An unexpected friend - ROS in apoptosis-induced compensatory proliferation: Implications for regeneration and cancer.Seminars in cell & developmental biology · 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Apoptosis-induced proliferation (AiP) maintains tissue homeostasis following massive stress-induced cell death. During this phenomenon, dying cells induce proliferation of the surviving cells to compensate for the tissue loss, and thus restore organ size. Along with wound healing and tissue regeneration, AiP also contributes to tumor repopulation following radiation or chemotherapy. There are several models of AiP. Using an "undead" AiP model that causes hyperplastic overgrowth of Drosophila epithelial tissue, we recently demonstrated that extracellular reactive oxygen species (eROS) are produced by undead epithelial cells, and are necessary for inducing AiP and overgrowth. Furthermore, hemocytes, the Drosophila blood cells, are seen adjacent to the undead epithelial tissue, and may secrete the TNF ortholog Eiger that signals through the TNF receptor to active Jun-N-terminal kinase (JNK) in the undead tissue and induce proliferation. We propose that undead epithelial tissue triggers an inflammatory response that resembles recruitment of macrophages to human epithelial tumors, and that these tumor-associated macrophages release signals for proliferation and tumor growth of the epithelium. This Extra View article summarizes these recent findings with a focus on the role of eROS for promoting regeneration and inflammation-induced tumorigenesis.
Indexed as
Identifiers
What OpenQuestion holds
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.