ArticleAmerican journal of physiology. Lung cellular and molecular physiology2025
Post-transcriptional regulation of IFI16 promotes inflammatory endothelial pathophenotypes observed in pulmonary arterial hypertension.
Article in American journal of physiology. Lung cellular and molecular physiology, 2025. 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.
- Pulmonary Hypertension Molecular Switch: HIF Signaling Pathway.Pulmonary circulation · 2026Review
- Genetic Evidence Supports a Potential Role of WTAP-related m6A Regulation in Vascular Dementia: Insights from Mendelian Randomization and Multi-omics Analyses.Journal of molecular neuroscience : MN · 2026Article
- Mitochondrial DNA-driven intercellular communication networks in post-infarction ventricular remodeling: the three-threshold model of cGAS-STING activation.Frontiers in immunology · 2026Review
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Mechanisms of T-cell Depletion in Tumors and Advances in Clinical Research.Biological procedures online · 2025Review
- Natural products targeting the immune-metabolic regulatory network in pulmonary hypertension: mechanisms, classification, and therapeutic prospects.Frontiers in pharmacology · 2025Review
- Post-transcriptional regulation of IFI16 promotes inflammatory endothelial pathophenotypes observed in pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2025Article
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Abstract
Pulmonary arterial hypertension (PAH) is a progressive disease driven by endothelial cell inflammation and dysfunction, resulting in the pathological remodeling of the pulmonary vasculature. Innate immune activation has been linked to PAH development; however, the regulation, propagation, and reversibility of the induction of inflammation in PAH are poorly understood. Here, we demonstrate the role of interferon-inducible protein 16 (IFI16), an innate immune sensor, as a modulator of endothelial inflammation in pulmonary hypertension, using human pulmonary artery endothelial cells (PAECs). Inflammatory stimulus of PAECs with IL-1β upregulates
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