Trial reportThe Journal of clinical investigation2015
Suppression of NLRX1 in chronic obstructive pulmonary disease.
Trial report in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 76 citations in OpenAlex.
- Ubiquitination-mediated degradation of NLRX1 drives metabolic vulnerability and accelerates intervertebral disc degeneration.Cell death and differentiation · 2026Article
- Article
- Repeated air pollution exposure predisposes to adverse outcomes from acute lung injury.Particle and fibre toxicology · 2026Article
- NLRX1 alleviates sepsis-induced acute lung injury by activating mitophagy and suppressing NLRP3 inflammasome activation.Frontiers in pharmacology · 2026Article
- Harnessing NLRX1: a new frontier in mitigating inflammation in pulmonary hypertension.Respiratory research · 2025Article
- Article
- The innate immune receptor NLRX1 is a novel required modulator for mPTP opening: implications for cardioprotection.Basic research in cardiology · 2025Article
- RNA m7G methylation regulators and targets significantly contribute to chronic obstructive pulmonary disease.Scientific reports · 2025Article
- NLRX1 Inhibits LPS-Induced Microglial Death via Inducing p62-Dependent HO-1 Expression, Inhibiting MLKL and Activating PARP-1.Antioxidants (Basel, Switzerland) · 2024Article
- NLRX1 Prevents M2 Macrophage Polarization and Excessive Renal Fibrosis in Chronic Obstructive Nephropathy.Cells · 2023Article
- NLRX1 knockdown attenuates pro-apoptotic signaling and cell death in pulmonary hyperoxic acute injury.Scientific reports · 2023Article
- Roles of inflammasomes in viral myocarditis.Frontiers in cellular and infection microbiology · 2023Review
- Immunometabolic rewiring of tubular epithelial cells in kidney disease.Nature reviews. Nephrology · 2022Review
- Polyphenols, flavonoids and inflammasomes: the role of cigarette smoke in COPD.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Host chitinase 3-like-1 is a universal therapeutic target for SARS-CoV-2 viral variants in COVID-19.eLife · 2022Article
- Somatic Mutations of Hematopoietic Cells Are an Additional Mechanism of Body Aging, Conducive to Comorbidity and Increasing Chronification of Inflammation.Biomedicines · 2022Review
- Impact of intracellular innate immune receptors on immunometabolism.Cellular & molecular immunology · 2022Review
- Sex-Biased Control of Inflammation and Metabolism by a Mitochondrial Nod-Like Receptor.Frontiers in immunology · 2022Article
- NLRX1 Deficiency Alters the Gut Microbiome and Is Further Exacerbated by Adherence to a Gluten-Free Diet.Frontiers in immunology · 2022Article
- Chitinase 3-like-1 is a therapeutic target that mediates the effects of aging in COVID-19.JCI insight · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 6 institutions in 2 countries.
Funding
Abstract
Cigarette smoke (CS) and viruses promote the inflammation and remodeling associated with chronic obstructive pulmonary disease (COPD). The MAVS/RIG-I-like helicase (MAVS/RLH) pathway and inflammasome-dependent innate immune pathways are important mediators of these responses. At baseline, the MAVS/RLH pathway is suppressed, and this inhibition must be reversed to engender tissue effects; however, the mechanisms that mediate activation and repression of the pathway have not been defined. In addition, the regulation and contribution of MAVS/RLH signaling in CS-induced inflammation and remodeling responses and in the development of human COPD remain unaddressed. Here, we demonstrate that expression of NLRX1, which inhibits the MAVS/RLH pathway and regulates other innate immune responses, was markedly decreased in 3 independent cohorts of COPD patients. NLRX1 suppression correlated directly with disease severity and inversely with pulmonary function, quality of life, and prognosis. In murine models, CS inhibited NLRX1, and CS-induced inflammation, alveolar destruction, protease induction, structural cell apoptosis, and inflammasome activation were augmented in NLRX1-deficient animals. Conversely, MAVS deficiency abrogated this CS-induced inflammation and remodeling. Restoration of NLRX1 in CS-exposed animals ameliorated alveolar destruction. These data support a model in which CS-dependent NLRX1 inhibition facilitates MAVS/RHL activation and subsequent inflammation, remodeling, protease, cell death, and inflammasome responses.
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.