ArticleThe Journal of biological chemistry2010
Enhancement of reactive oxygen species production and chlamydial infection by the mitochondrial Nod-like family member NLRX1.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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
84 citing papers in PubMed, 145 citations in OpenAlex.
- NLRX1 emerges as the only observed essential regulator of the mPTP, challenging mPTP inhibition as a valid target of cardioprotection.Basic research in cardiology · 2026Review
- Article
- Bacterial Infections Role in Gynecological Cancers Development: Narrative Review.Cancer reports (Hoboken, N.J.) · 2026Review
- NLRX1 Drives Prostate Cancer Progression Through Activation of AKT and ERK Signaling Pathways.International journal of biological sciences · 2026Article
- Harnessing NLRX1: a new frontier in mitigating inflammation in pulmonary hypertension.Respiratory research · 2025Article
- The critical role of the ZBP1-NINJ1 axis and IRF1/IRF9 in ethanol-induced cell death, PANoptosis, and alcohol-associated liver disease.bioRxiv : the preprint server for biology · 2025Article
- Altering the redox status ofeLife · 2025Article
- Pattern Recognition by NOD-Like Receptors.Advances in experimental medicine and biology · 2025Review
- Decoding mitochondrial DNA damage and repair associated withFrontiers in cellular and infection microbiology · 2024Review
- Cellular Context Dictates the Suppression or Augmentation of Triple-Negative Mammary Tumor Metastasis by NLRX1.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- A trans-kingdom T6SS effector induces the fragmentation of the mitochondrial network and activates innate immune receptor NLRX1 to promote infection.Nature communications · 2023Article
- The role of NOD-like receptors in innate immunity.Frontiers in immunology · 2023Review
- Insights Into Mitochondrial Dynamics in Chlamydial Infection.Frontiers in cellular and infection microbiology · 2022Review
- Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far.Frontiers in oncology · 2022Review
- Mitochondria as a Cellular Hub in Infection and Inflammation.International journal of molecular sciences · 2021Review
- Bacteria-Cancer Interface: Awaiting the Perfect Storm.Pathogens (Basel, Switzerland) · 2021Review
- NLR in eXile: Emerging roles of NLRX1 in immunity and human disease.Immunology · 2021Review
- Natural genetic variation determines microglia heterogeneity in wild-derived mouse models of Alzheimer's disease.Cell reports · 2021Article
- Role of NLRs in the Regulation of Type I Interferon Signaling, Host Defense and Tolerance to Inflammation.International journal of molecular sciences · 2021Review
- Focusing on the Cell Type Specific Regulatory Actions of NLRX1.International journal of molecular sciences · 2021Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
Chlamydia trachomatis infections cause severe and irreversible damage that can lead to infertility and blindness in both males and females. Following infection of epithelial cells, Chlamydia induces production of reactive oxygen species (ROS). Unconventionally, Chlamydiae use ROS to their advantage by activating caspase-1, which contributes to chlamydial growth. NLRX1, a member of the Nod-like receptor family that translocates to the mitochondria, can augment ROS production from the mitochondria following Shigella flexneri infections. However, in general, ROS can also be produced by membrane-bound NADPH oxidases. Given the importance of ROS-induced caspase-1 activation in growth of the chlamydial vacuole, we investigated the sources of ROS production in epithelial cells following infection with C. trachomatis. In this study, we provide evidence that basal levels of ROS are generated during chlamydial infection by NADPH oxidase, but ROS levels, regardless of their source, are enhanced by an NLRX1-dependent mechanism. Significantly, the presence of NLRX1 is required for optimal chlamydial growth.
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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.