Microglial immunosurveillance after ischemic stroke: dynamic phenotypes, neurovascular interactions, and therapeutic opportunities.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic concepts without systematic search or meta-analytic data
PubMed 42639315 · doi:10.3389/fimmu.2026.1893074
What was done
This narrative review synthesized literature on microglial immunosurveillance, phenotypic transitions, and neurovascular interactions following ischemic stroke, examining recent single-cell transcriptomic insights, systemic immune connections, and potential therapeutic targets.
What was found
The abstract reports no quantitative data or effect sizes. It qualitatively describes that microglia transition rapidly from homeostatic surveillance to dynamic states that can either support blood-brain barrier integrity and repair or exacerbate inflammation, oxidative stress, inflammasome signaling, and synaptic pruning. It notes that single-cell transcriptomics challenges the binary M1/M2 model and details interactions between microglia and various neurovascular and peripheral immune cell types.
Why it matters
The review underscores that effective stroke therapeutics must move away from broad neuroinflammatory suppression toward context- and stage-specific modulation of distinct microglial phenotypes and metabolic pathways.
Limits
As a narrative review, it contains no primary human clinical data, quantitative meta-analysis, or formal risk-of-bias assessment. Clinical translation is noted to be constrained by narrow therapeutic windows, high patient heterogeneity, difficulty differentiating resident microglia from infiltrating peripheral macrophages, and an absence of validated biomarkers.
Cited by
- supports Microglial cells support blood-brain barrier maintenance, but this maintenance is impaired when microglia switch to the pro-inflammatory M1 phenotype.