ArticleFrontiers in immunology2016
Formyl Peptide Receptor Activation Elicits Endothelial Cell Contraction and Vascular Leakage.
Article in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Impact of early albumin therapy on 28-day survival in ICU patients with septic shock concurrent hypoalbuminemia: a retrospective analysis of combined clinical datasets.World journal of emergency medicine · 2026Article
- Hemodynamics and matrix stiffness shape the pathogenicity of SPP1Frontiers in immunology · 2026Review
- Plasminogen System in the Pathophysiology of Sepsis: Upcoming Biomarkers.International journal of molecular sciences · 2023Review
- Targeting cytokine-like protein FAM3D lowers blood pressure in hypertension.Cell reports. Medicine · 2023Article
- Role of Mitochondria-Derived Danger Signals Released After Injury in Systemic Inflammation and Sepsis.Antioxidants & redox signaling · 2021Review
- Stimulation of the Migration and Expansion of Adult Mouse Neural Stem Cells by the FPR2-Specific Peptide WKYMVm.Life (Basel, Switzerland) · 2021Article
- FPR-1 (Formyl Peptide Receptor-1) Activation Promotes Spontaneous, Premature Hypertension in Dahl Salt-Sensitive Rats.Hypertension (Dallas, Tex. : 1979) · 2021Article
- The Novel Small-molecule Annexin-A1 Mimetic, Compound 17b, Elicits Vasoprotective Actions in Streptozotocin-induced Diabetic Mice.International journal of molecular sciences · 2020Article
- Targeting Endothelial Barrier Dysfunction Caused by Circulating Bacterial and Mitochondrial N-Formyl Peptides With Deformylase.Frontiers in immunology · 2019Article
- Mitochondria in innate immune signaling.Translational research : the journal of laboratory and clinical medicine · 2018Review
- DT-13 Ameliorates TNF-α-Induced Vascular Endothelial HyperpermeabilityFrontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The major pathophysiological characteristic of systemic inflammatory response syndrome (SIRS) and sepsis is the loss of control of vascular tone and endothelial barrier dysfunction. These changes are attributed to pro-inflammatory mediators. It has been proposed that in patients and rats without infection, cell components from damaged tissue are the primary instigators of vascular damage. Mitochondria share several characteristics with bacteria, and when fragments of mitochondria are released into the circulation after injury, they are recognized by the innate immune system. N-Formyl peptides are common molecular signatures of bacteria and mitochondria and are known to play a role in the initiation of inflammation by activating the formyl peptide receptor (FPR). We have demonstrated that infusion of mitochondrial N-formyl peptides (F-MIT) leads to sepsis-like symptoms, including vascular leakage. We have also observed that F-MIT, via FPR activation, elicits changes in cytoskeleton-regulating proteins in endothelial cells. Therefore, we hypothesize that these FPR-mediated changes in cytoskeleton can cause endothelial cell contraction and, consequently vascular leakage. Here, we propose that endothelial FPR is a key contributor to impaired barrier function in SIRS and sepsis patients following trauma.
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Registered trials
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