ArticleThe Journal of clinical investigation2020
IL-1β suppression of VE-cadherin transcription underlies sepsis-induced inflammatory lung injury.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 158 papers.
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Who cites it
158 citing papers in PubMed, 216 citations in OpenAlex.
- Mechanisms and therapeutic strategies of pyroptosis in sepsis‑induced acute lung injury (Review).International journal of molecular medicine · 2026Review
- Tetracycline-loaded nanomotors target neutrophil activation and oxidative stress in acute lung injury.iScience · 2026Article
- Mild photothermal therapy ameliorates neurogenic bladder after sacral spinal cord injury via multi-target effects.Materials today. Bio · 2026Article
- TRPV4/IP3R-1-mediated endothelial pyroptosis drives pulmonary microvascular endothelial permeability in endotoxin-induced acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Diffuse alveolar damage, acute respiratory distress syndrome (ARDS), and non-cardiogenic pulmonary edema. Part 1: ARDS endotypes, including systemic inflammatory response syndrome and sepsis, with dog and cat examples.Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · 2026Review
- Lappaconitine hydrobromide prevents NLRP3-GSDMD-mediated pyroptosis to alleviate sepsis-induced acute lung injury by enhancing NR1H3.Journal of pharmaceutical analysis · 2026Article
- Karacoline attenuates sepsis-induced acute lung injury by suppressing apoptosis via PPARγ-associated inhibition of JNK/ERK MAPK signaling.Respiratory research · 2026Article
- MicroRNA-125a-5p promotes NLRP3/caspase-1/GSDMD pathway-mediated pyroptosis in endothelial cells during Kawasaki disease.Scientific reports · 2026Article
- Incorporating WGCNA and Machine Learning to Identify ADAP2 as a Critical Efferocytosis-Related Gene in Sepsis.Pathogens (Basel, Switzerland) · 2026Article
- C-Type Natriuretic Peptide Preserves Vascular and Cardiac Function in Sepsis.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Treatment of heterotopic ossification via inhibiting the MMP-2/CDH5 axis through oral delivery of network pharmacology-predicted Chinese medicine.Materials today. Bio · 2026Article
- The gut-lung axis in ARDS: beyond microbial translocation.Respiratory research · 2026Review
- IL-36 activates neutrophil extracellular traps and exacerbates LPS-induced ARDS in mice.Scientific reports · 2026Article
- Phosphodiesterase signaling in asthma: mechanistic insights and emerging therapeutic strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- PROK2 defines a pathogenic neutrophil subset and serves as a clinical indicator of neutrophilic inflammation in COPD.Respiratory research · 2026Article
- Endothelial NEDD4L exacerbates acute lung injury by targeting A20 for ubiquitination degradation.Respiratory research · 2026Article
- Cadherin-11 serves as a novel receptor for Fusobacterium nucleatum adhesin FadA to exacerbate pulmonary inflammation.PLoS pathogens · 2026Article
- HIF-1 A-Mediated Lactate Metabolism Confers Ferroptosis Resistance in M1 Macrophages Through Histone Lactylation During Acute Lung Injury.Inflammation · 2026Article
- USP19 alleviates LPS-induced acute lung injury via inhibiting TAK1 activation.Biology direct · 2026Article
- STING-ERO1 signaling exacerbates PARylation-mediated parthanatos in sepsis.Cell communication and signaling : CCS · 2026Article
98 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Unchecked inflammation is a hallmark of inflammatory tissue injury in diseases such as acute respiratory distress syndrome (ARDS). Yet the mechanisms of inflammatory lung injury remain largely unknown. Here we showed that bacterial endotoxin lipopolysaccharide (LPS) and cecal ligation and puncture-induced (CLP-induced) polymicrobial sepsis decreased the expression of transcription factor cAMP response element binding (CREB) in lung endothelial cells. We demonstrated that endothelial CREB was crucial for VE-cadherin transcription and the formation of the normal restrictive endothelial adherens junctions. The inflammatory cytokine IL-1β reduced cAMP generation and CREB-mediated transcription of VE-cadherin. Furthermore, endothelial cell-specific deletion of CREB induced lung vascular injury whereas ectopic expression of CREB in the endothelium prevented the injury. We also observed that rolipram, which inhibits type 4 cyclic nucleotide phosphodiesterase-mediated (PDE4-mediated) hydrolysis of cAMP, prevented endotoxemia-induced lung vascular injury since it preserved CREB-mediated VE-cadherin expression. These data demonstrate the fundamental role of the endothelial cAMP-CREB axis in promoting lung vascular integrity and suppressing inflammatory injury. Therefore, strategies aimed at enhancing endothelial CREB-mediated VE-cadherin transcription are potentially useful in preventing sepsis-induced lung vascular injury in ARDS.
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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.