Fibrinogen signal transduction in the nervous system.
Level 5 - mechanism / opinion, no new human data
Narrative review describing biological mechanisms without clinical trial or human observational data
PubMed 19630789 · doi:10.1111/j.1538-7836.2009.03438.x
What was done
This is a narrative review examining the mechanisms by which extravasated fibrinogen signals through cell-specific receptors in the nervous system following blood-brain barrier disruption.
What was found
The abstract reports purely qualitative mechanistic pathways and contains no numerical data or effect sizes. Fibrinogen acts as a ligand for the CD11b/CD18 integrin receptor on microglia to activate Akt and Rho, and binds the alphavbeta3 integrin on neurons to induce epidermal growth factor (EGF) receptor phosphorylation, promoting inflammation and inhibiting neurite outgrowth.
Why it matters
It characterizes fibrinogen as an active driver of neuroinflammation and neurite inhibition rather than an inert marker of vascular leakage, highlighting receptor-ligand interactions as candidate drug targets.
Limits
This is a narrative review with no systematic methodology or primary human clinical data. The abstract provides no sample sizes, effect magnitudes, or specific disease-model parameters.
Cited by
- supports Fibrinogen binds to CD11b receptors on microglia, triggering an inflammatory reaction in the brain.