ArticleThe Journal of experimental medicine2023
Host factor TIMP1 sustains long-lasting myeloid-biased hematopoiesis after severe infection.
Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Diabetes and Immunosuppression Drive Distinct Patterns ofbioRxiv : the preprint server for biology · 2026Article
- Inflammatory metabolite 7α,25-OHC promotes TIMP1 expression in COVID-19 monocytes through synergy effect of SMARCC1/JUND/H3K27ac.Cellular and molecular life sciences : CMLS · 2025Article
- Unsupervised Classification of the Host Response Identifies Dominant Pathobiological Signatures of Sepsis in Sub-Saharan Africa.American journal of respiratory and critical care medicine · 2025Article
- Suppression of thrombospondin-1-mediated inflammaging prolongs hematopoietic health span.Science immunology · 2025Article
- Bioinformatics Analysis and Identification of Ferroptosis-Related Gene TIMP1 as a Potential Biomarker of Asthma.Journal of inflammation research · 2025Article
- Enhanced resistance toFrontiers in pharmacology · 2025Article
- CDK6-mediated endothelial cell cycle acceleration drives arteriovenous malformations in hereditary hemorrhagic telangiectasia.Nature cardiovascular research · 2024Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Infection is able to promote innate immunity by enhancing a long-term myeloid output even after the inciting infectious agent has been cleared. However, the mechanisms underlying such a regulation are not fully understood. Using a mouse polymicrobial peritonitis (sepsis) model, we show that severe infection leads to increased, sustained myelopoiesis after the infection is resolved. In post-infection mice, the tissue inhibitor of metalloproteinases 1 (TIMP1) is constitutively upregulated. TIMP1 antagonizes the function of ADAM10, an essential cleavage enzyme for the activation of the Notch signaling pathway, which suppresses myelopoiesis. While TIMP1 is dispensable for myelopoiesis under the steady state, increased TIMP1 enhances myelopoiesis after infection. Thus, our data establish TIMP1 as a molecular reporter of past infection in the host, sustaining hyper myelopoiesis and serving as a potential therapeutic target for modulating HSPC cell fate.
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