ReviewCardiovascular research2015
Intracellular signalling during neutrophil recruitment.
Review in Cardiovascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 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
81 citing papers in PubMed, 156 citations in OpenAlex.
- Review
- Genetic regulation of AIF1 shapes immune and liver injury profiles in chronic alcohol use.JCI insight · 2026Article
- Sitagliptin Modulates Functional and Phenotypic Properties of Human Neutrophils Under Normal- and High-Glucose Conditions In Vitro.Molecules (Basel, Switzerland) · 2026Article
- Role of neutrophils in regulating vascular permeability in inflammatory and autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Article
- From inflammatory effectors to tissue sculptors: non-canonical functions of neutrophils in repair, barrier remodelling and fibrosis.Frontiers in immunology · 2026Review
- The applicability of the MigratestBMC veterinary research · 2025Article
- A nano-immuno-cruise delivery system encapsulated lipid-integrated bilayer ameliorate acute lung injury by interfering neutrophil infiltration.Materials today. Bio · 2025Article
- Palmitic acid and palmitoylation in cancer: Understanding, insights, and challenges.Innovation (Cambridge (Mass.)) · 2025Review
- Targeting CXCR2 signaling in inflammatory lung diseases: neutrophil-driven inflammation and emerging therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Article
- Structural and functional brain correlates of the neutrophil- and monocyte-to-lymphocyte ratio in neuropsychiatric disorders.Brain, behavior, & immunity - health · 2025Article
- 4-Phenyl Butyric Acid (4-PBA) Suppresses Neutrophil Recruitment in a Murine Model of Acute Perinatal Inflammation.Journal of immunology research · 2025Article
- INTEGRIN FUNCTION IN LEUKOCYTE-MEDIATED INFLAMMATION-ACTINOPATHIES IN IMMUNE DISEASES.Transactions of the American Clinical and Climatological Association · 2025Review
- Molecular mechanisms of neutrophil regulatory network in anti-Candida infection.Frontiers in immunology · 2025Review
- Cerebral Endothelial CXCR2 Promotes Neutrophil Transmigration into Central Nervous System in LPS-Induced Septic Encephalopathy.Biomedicines · 2024Article
- Tumor-neutrophil cross talk orchestrates the tumor microenvironment to determine the bladder cancer progression.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Neutrophil Extracellular DNA Traps in Response to Infection or Inflammation, and the Roles of Platelet Interactions.International journal of molecular sciences · 2024Review
- Immuno-inflammatory pathogenesis in ischemic heart disease: perception and knowledge for neutrophil recruitment.Frontiers in immunology · 2024Review
- Neutrophil attachment via Mac-1 (Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
Abstract
Recruitment of leucocytes such as neutrophils to the extravascular space is a critical step of the inflammation process and plays a major role in the development of various diseases including several cardiovascular diseases. Neutrophils themselves play a very active role in that process by sensing their environment and responding to the extracellular cues by adhesion and de-adhesion, cellular shape changes, chemotactic migration, and other effector functions of cell activation. Those responses are co-ordinated by a number of cell surface receptors and their complex intracellular signal transduction pathways. Here, we review neutrophil signal transduction processes critical for recruitment to the site of inflammation. The two key requirements for neutrophil recruitment are the establishment of appropriate chemoattractant gradients and the intrinsic ability of the cells to migrate along those gradients. We will first discuss signalling steps required for sensing extracellular chemoattractants such as chemokines and lipid mediators and the processes (e.g. PI3-kinase pathways) leading to the translation of extracellular chemoattractant gradients to polarized cellular responses. We will then discuss signal transduction by leucocyte adhesion receptors (e.g. tyrosine kinase pathways) which are critical for adhesion to, and migration through the vessel wall. Finally, additional neutrophil signalling pathways with an indirect effect on the neutrophil recruitment process, e.g. through modulation of the inflammatory environment, will be discussed. Mechanistic understanding of these pathways provide better understanding of the inflammation process and may point to novel therapeutic strategies for controlling excessive inflammation during infection or tissue damage.
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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.