ArticleNature microbiology2025
A single-cell transcriptomic atlas reveals senescence and inflammation in the post-tuberculosis human lung.
Article in Nature microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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.
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Who cites it
11 citing papers in PubMed.
- Host-pathogen interactions in tuberculosis: from immunological mechanisms to translational applications.Cell insight · 2026Review
- Does Tuberculosis Leave a Thromboinflammatory Memory After Cure? A Narrative Review with a Conceptual Framework on Hypercoagulability, Cellular Reservoirs, and Extracellular Vesicle Signaling.International journal of molecular sciences · 2026Review
- Elimination of senescent cells with senolytic drugs as adjunctive host-directed therapy reduces tuberculosis progression in mice.Nature communications · 2026Article
- Single-Cell and Spatial Omics: Methods and Applications.MedComm · 2026Review
- The Emerging Role of Immunothrombosis in the Control and Pathogenesis of Mycobacterium tuberculosis.The Journal of infectious diseases · 2026Review
- Antimicrobial resistance dynamics inBiochemistry and biophysics reports · 2026Article
- Genetically engineered senescence-resistant human mesenchymal progenitor cells promote spinal cord injury repair.Life medicine · 2026Article
- Article
- A Year in Review on Tuberculosis and Non-tuberculous Mycobacteria Disease: A 2026 Update for Clinicians and Scientists.Pathogens & immunity · 2026Review
- Review
- The drug discovery and therapeutic nano-strategies targeting cellular senescence.Materials today. Bio · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with a history of Mycobacterium tuberculosis infection often suffer from irreversible and progressive pulmonary damage, yet the underlying mechanisms are not fully understood. Here we conducted single-cell transcriptomic analysis of human lung tissues including 19 post-tuberculosis lung tissues and 13 matched normal lung samples as controls, focusing on areas within and surrounding tuberculosis lesions. We identified tuberculosis-associated molecular signatures across various cell types, including gene expression patterns associated with senescence, inflammation, fibrosis and apoptosis. We observed increased vascular inflammation as a key feature of lung tissues following tuberculosis. Signatures of decreased FOXO3 signalling and increased NF-κB-dependent thromboinflammation were validated by showing that small interfering RNA silencing of FOXO3 and thrombin treatment exacerbated senescence and inflammation in pulmonary endothelial cells. These findings provide insight into the mechanisms contributing to post-tuberculosis pulmonary damage and suggest potential therapeutic targets for alleviating lung impairment in these patients.
Indexed as
Identifiers
40659921What Socratic 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 Socratic graph.