ArticleJCI insight2022
Impairing RAGE signaling promotes survival and limits disease pathogenesis following SARS-CoV-2 infection in mice.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 24 citations in OpenAlex.
- Deconstructing the RAGE signaling maze: the molecular key to opening a new dimension of ovarian anti-aging.Experimental & molecular medicine · 2026Review
- Type 1 diabetes mellitus prevention: present and future.Nature reviews. Endocrinology · 2025Review
- Role of the receptor for advanced glycation end products in the severity of SARS-CoV-2 infection in diabetic patients.Diabetology international · 2024Review
- RAGE Is a Receptor for SARS-CoV-2 N Protein and Mediates N Protein-induced Acute Lung Injury.American journal of respiratory cell and molecular biology · 2023Article
- Targeting 2-Oxoglutarate-Dependent Dioxygenases Promotes Metabolic Reprogramming That Protects against Lethal SARS-CoV-2 Infection in the K18-hACE2 Transgenic Mouse Model.ImmunoHorizons · 2023Article
- RAGE Inhibitors in Neurodegenerative Diseases.Biomedicines · 2023Review
- Self-DNA driven inflammation in COVID-19 and after mRNA-based vaccination: lessons for non-COVID-19 pathologies.Frontiers in immunology · 2023Article
- RAGE signaling regulates the progression of diabetic complications.Frontiers in pharmacology · 2023Review
- Route of Francisella tularensis infection informs spatiotemporal metabolic reprogramming and inflammation in mice.PloS one · 2023Article
- Contribution of Lipid Mediators in Divergent Outcomes following Acute Bacterial and Viral Lung Infections in the Obese Host.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Advanced Glycation End Products in Health and Disease.Microorganisms · 2022Review
- Evolution and diabetic vasculopathy.Journal of diabetes investigation · 2022Article
- The RAGE/DIAPH1 Signaling Axis & Implications for the Pathogenesis of Diabetic Complications.International journal of molecular sciences · 2022Review
- Mechanical control of innate immune responses against viral infection revealed in a human lung alveolus chip.Nature communications · 2022Article
- Glycation and a Spark of ALEs (Advanced Lipoxidation End Products) - Igniting RAGE/Diaphanous-1 and Cardiometabolic Disease.Frontiers in cardiovascular medicine · 2022Review
- Peripheral Pathways to Neurovascular Unit Dysfunction, Cognitive Impairment, and Alzheimer's Disease.Frontiers in aging neuroscience · 2022Review
- RAGE pathway activation and function in chronic kidney disease and COVID-19.Frontiers in medicine · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Cellular and molecular mechanisms driving morbidity following SARS-CoV-2 infection have not been well defined. The receptor for advanced glycation end products (RAGE) is a central mediator of tissue injury and contributes to SARS-CoV-2 disease pathogenesis. In this study, we temporally delineated key cell and molecular events leading to lung injury in mice following SARS-CoV-2 infection and assessed efficacy of therapeutically targeting RAGE to improve survival. Early following infection, SARS-CoV-2 replicated to high titers within the lungs and evaded triggering inflammation and cell death. However, a significant necrotic cell death event in CD45- populations, corresponding with peak viral loads, was observed on day 2 after infection. Metabolic reprogramming and inflammation were initiated following this cell death event and corresponded with increased lung interstitial pneumonia, perivascular inflammation, and endothelial hyperplasia together with decreased oxygen saturation. Therapeutic treatment with the RAGE antagonist FPS-ZM1 improved survival in infected mice and limited inflammation and associated perivascular pathology. Together, these results provide critical characterization of disease pathogenesis in the mouse model and implicate a role for RAGE signaling as a therapeutic target to improve outcomes following SARS-CoV-2 infection.
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.