ArticleAging and disease2023
Influenza Virus-Induced Paracrine Cellular Senescence of the Lung Contributes to Enhanced Viral Load.
Article in Aging and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
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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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Cellular senescence in acute human infectious disease: a systematic review.Frontiers in aging · 2024Pooled it
- Experimental evolution of phage K enhances antibacterial activity against USA300 MRSA in lung infection models.Emerging microbes & infections · 2026Article
- Remodeling of innate antiviral immunity in aging.Cell insight · 2026Review
- Article
- Hippo pathway activation drives fibrogenic remodelling in influenza A virus-infected lung fibroblasts.ERJ open research · 2026Article
- Cellular senescence dysregulates antiviral interferon responses in idiopathic pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Senolytic Treatment Reduces Acute and Chronic Lung Inflammation in an Aged Mouse Model of Influenza.Aging cell · 2026Article
- Inhibitory effect of three components derived from Salvia miltiorrhiza against human cytomegalovirus.Virology journal · 2026Article
- Article
- SARS-CoV-2 spike triggers TLR7-dependent endolysosome dysfunction and senescence in human astrocytes.Journal of neuroinflammation · 2025Article
- Senescent cells promote viral infection-associated inflammation and tissue damage through a robust NF-κB pathway.Cell communication and signaling : CCS · 2025Article
- ApoD mediates age-associated increase in vulnerability to influenza virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Virus-Induced Cellular Senescence Causes Pulmonary Sequelae Post-Influenza Infection.Aging cell · 2025Article
- A Human Immuno-Lung Organoid Model to Study Macrophage-Mediated Lung Cell Senescence Upon SARS-CoV-2 Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- High-fat diet impairs microbial metabolite production and aggravates influenza A infection.Cell communication and signaling : CCS · 2025Article
- Aging shapes infection profiles of influenza A virus and SARS-CoV-2 in human precision-cut lung slices.Respiratory research · 2025Article
- A skin organoid-based infection platform identifies an inhibitor specific for HFMD.Nature communications · 2025Article
- Review
- Age-related STING suppression in macrophages contributes to increased viral load during influenza a virus infection.Immunity & ageing : I & A · 2024Article
- FBXL19 in endothelial cells protects the heart from influenza A infection by enhancing antiviral immunity and reducing cellular senescence programs.American journal of physiology. Heart and circulatory physiology · 2024Article
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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is a major risk factor associated with increased morbidity and mortality rates observed during respiratory infections. In this study, we investigated the role of influenza virus infections in the establishment of premature cellular senescence and paracrine macrophage-activated inflammation. We observed in our murine model a premature aging by the appearance of senescent cells in the lungs after 21 d of influenza A virus infection. By using murine ex vivo lung models, the influence of TNF-α on the establishment of cellular senescence was detectable. Our findings were proven by using conditioned media of infected human monocyte-derived macrophages on primary lung fibroblasts. Here, a distinct expression of senescence-associated parameters could be confirmed. Furthermore, senescent cells in the lungs strongly influenced subsequent viral infections. Our data demonstrated a higher viral load in senescent primary lung fibroblasts, indicating an intracellular effect on viral replication. Transcriptomic data revealed an increased regulation of JAK/STAT signaling in senescent IAV-infected cells accompanied with increased TRAIL expression. Additionally, senescent cells indicating low pH values, accelerating viral replication. Our study provides new insights into pathomechanisms of virus-induced cellular senescence. Hence, IAV infection induces premature senescence and subsequent infections in senescent cells lead to an increased viral replication.
Identifiers
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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.