ArticleAmerican journal of physiology. Lung cellular and molecular physiology2022
Pim-1 kinase is a positive feedback regulator of the senescent lung fibroblast inflammatory secretome.
Article in American journal of physiology. Lung cellular and molecular physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- PIM1 Inhibition Alleviates Aspergillus fumigatus Keratitis by Regulating DDX41-Mediated STING Signaling Pathway.Investigative ophthalmology & visual science · 2026Article
- The Sixth Annual Symposium of the Midwest Aging Consortium.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026Article
- CBX7 regulates chemotherapy-induced senescence-like growth arrest in multiple myeloma via the ERK/STAT3/PIM1 axis.Journal of translational medicine · 2025Article
- Optimized Synthetic Flavonols Support Senescence Clearance and Lung Fibrosis Resolution.ACS pharmacology & translational science · 2025Article
- Development and Application of a Senolytic Predictor for Discovery of Novel Senolytic Compounds and Herbs.Molecules (Basel, Switzerland) · 2025Article
- Differential susceptibility and role for senescence in CART cells based on costimulatory domains.Molecular cancer · 2025Article
- Comprehensive assessment of disulfidptosis-related long non-coding RNA index as biomarkers for predicting clinical outcomes and immune microenvironment in pancreatic cancer.Translational cancer research · 2025Article
- NR2F2 alleviates pulmonary fibrosis by inhibition of epithelial cell senescence.Respiratory research · 2024Article
- PIM1 signaling in immunoinflammatory diseases: an emerging therapeutic target.Frontiers in immunology · 2024Review
- Cellular Senescence: A Troy Horse in Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 2 countries.
Funding
Abstract
Cellular senescence is emerging as a driver of idiopathic pulmonary fibrosis (IPF), a progressive and fatal disease with limited effective therapies. The senescence-associated secretory phenotype (SASP), involving the release of inflammatory cytokines and profibrotic growth factors by senescent cells, is thought to be a product of multiple cell types in IPF, including lung fibroblasts. NF-κB is a master regulator of the SASP, and its activity depends on the phosphorylation of p65/RelA. The purpose of this study was to assess the role of Pim-1 kinase as a driver of NF-κB-induced production of inflammatory cytokines from low-passage IPF fibroblast cultures displaying markers of senescence. Our results demonstrate that Pim-1 kinase phosphorylates p65/RelA, activating NF-κB activity and enhancing IL-6 production, which in turn amplifies the expression of
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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.