ReviewShock (Augusta, Ga.)2013
Protein kinase C and acute respiratory distress syndrome.
Review in Shock (Augusta, Ga.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Plasma Lipidomics Identify Pathways Linked to Acute Lung Injury in a Porcine One-Lung Ventilation Surgery Model.International journal of molecular sciences · 2026Article
- Mac-1 blockade impedes adhesion-dependent neutrophil extracellular trap formation and ameliorates lung injury in LPS-induced sepsis.Frontiers in immunology · 2025Article
- Special Issue: "Molecular Dynamics Simulations and Structural Analysis of Protein Domains".International journal of molecular sciences · 2024Article
- Article
- An Update on Protein Kinases as Therapeutic Targets-Part I: Protein Kinase C Activation and Its Role in Cancer and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Review
- Association of soluble receptor for advanced glycation end-products (sRAGE) serum on COVID-19 severity: A cross-sectional study.Annals of medicine and surgery (2012) · 2022Article
- Emerging Approaches to Understanding Microvascular Endothelial Heterogeneity: A Roadmap for Developing Anti-Inflammatory Therapeutics.International journal of molecular sciences · 2021Review
- Experimental Approaches to Evaluate Leukocyte-Endothelial Cell Interactions in Sepsis and Inflammation.Shock (Augusta, Ga.) · 2020Article
- Protein kinase C-delta inhibition is organ-protective, enhances pathogen clearance, and improves survival in sepsis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Neutrophil-endothelial interactions of murine cells is not a good predictor of their interactions in human cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Protein Kinase C-Delta (PKCδ) Tyrosine Phosphorylation is a Critical Regulator of Neutrophil-Endothelial Cell Interaction in Inflammation.Shock (Augusta, Ga.) · 2019Article
- The Role of Tyrosine Phosphorylation of Protein Kinase C Delta in Infection and Inflammation.International journal of molecular sciences · 2019Review
- Stromal-Interacting Molecule 1 (Stim1)/Orai1 Modulates Endothelial Permeability in Ventilator-Induced Lung Injury.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Chinese liquor extract enhances inflammation resistance in RAW 264.7 and reduces aging inRSC advances · 2018Article
- Protein kinase C-delta inhibition protects blood-brain barrier from sepsis-induced vascular damage.Journal of neuroinflammation · 2018Article
- Early application of low-dose glucocorticoid improves acute respiratory distress syndrome: A meta-analysis of randomized controlled trials.Experimental and therapeutic medicine · 2017Article
- Protein Kinase Cζ Inhibitor Promotes Resolution of Bleomycin-Induced Acute Lung Injury.American journal of respiratory cell and molecular biology · 2016Article
- A novel microfluidic assay reveals a key role for protein kinase C δ in regulating human neutrophil-endothelium interaction.Journal of leukocyte biology · 2016Article
- The role of stretch-activated ion channels in acute respiratory distress syndrome: finally a new target?American journal of physiology. Lung cellular and molecular physiology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The acute respiratory distress syndrome (ARDS) is a major public health problem and a leading source of morbidity in intensive care units. Lung tissue in patients with ARDS is characterized by inflammation, with exuberant neutrophil infiltration, activation, and degranulation that is thought to initiate tissue injury through the release of proteases and oxygen radicals. Treatment of ARDS is supportive primarily because the underlying pathophysiology is poorly understood. This gap in knowledge must be addressed to identify urgently needed therapies. Recent research efforts in anti-inflammatory drug development have focused on identifying common control points in multiple signaling pathways. The protein kinase C (PKC) serine-threonine kinases are master regulators of proinflammatory signaling hubs, making them attractive therapeutic targets. Pharmacological inhibition of broad-spectrum PKC activity and, more importantly, of specific PKC isoforms (as well as deletion of PKCs in mice) exerts protective effects in various experimental models of lung injury. Furthermore, PKC isoforms have been implicated in inflammatory processes that may be involved in the pathophysiologic changes that result in ARDS, including activation of innate immune and endothelial cells, neutrophil trafficking to the lung, regulation of alveolar epithelial barrier functions, and control of neutrophil proinflammatory and prosurvival signaling. This review focuses on the mechanistic involvement of PKC isoforms in the pathogenesis of ARDS and highlights the potential of developing new therapeutic paradigms based on the selective inhibition (or activation) of specific PKC isoforms.
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What OpenQuestion holds
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.