ArticleThe Journal of cell biology2023
A PI3K-calcium-Nox axis primes leukocyte Nrf2 to boost immune resilience and limit collateral damage.
Article in The Journal of cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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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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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Chiral FeBioactive materials · 2026Article
- CircRNA-encoded protein fine-tunes ROS homeostasis and engages conserved JAK-STAT antiviral defenses inJournal of virology · 2026Article
- Activation of AKT via a dual mechanism enhances the susceptibility of melanoma cells to glucose deprivation.Cell death & disease · 2025Article
- Lutein protection against doxorubicin-induced liver damage in rats is associated with inhibition of oxido-inflammatory stress and modulation of Beclin-1/mTOR activities.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Biological resilience in health and disease.Disease models & mechanisms · 2024Review
- Understanding the diversity and dynamics of in vivo efferocytosis: Insights from the fly embryo.Immunological reviews · 2023Review
- Macrophage Nrf 2 the rescue.The Journal of cell biology · 2023Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Phagosomal reactive oxygen species (ROS) are strategically employed by leukocytes to kill internalized pathogens and degrade cellular debris. Nevertheless, uncontrolled oxidant bursts could cause serious collateral damage to phagocytes or other host tissues, potentially accelerating aging and compromising host viability. Immune cells must, therefore, activate robust self-protective programs to mitigate these undesired effects, and yet allow crucial cellular redox signaling. Here, we dissect in vivo the molecular nature of these self-protective pathways, their precise mode of activation, and physiological effects. We reveal Drosophila embryonic macrophages activate the redox-sensitive transcription factor Nrf2 upon corpse engulfment during immune surveillance, downstream of calcium- and PI3K-dependent ROS release by phagosomal Nox. By transcriptionally activating the antioxidant response, Nrf2 not only curbs oxidative damage but preserves vital immune functions (including inflammatory migration) and delays the acquisition of senescence-like features. Strikingly, macrophage Nrf2 also acts non-autonomously to limit ROS-induced collateral damage to surrounding tissues. Cytoprotective strategies may thus offer powerful therapeutic opportunities for alleviating inflammatory or age-related diseases.
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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.