Growth Factors in Ischemic Stroke Recovery

Growth factors are soluble proteins that orchestrate cell survival, proliferation and repair following cerebral ischaemia. Endogenous factors such as insulin-like growth factor-1 (IGF-1), fibroblast growth factors (FGFs) and brain-derived neurotrophic factor (BDNF) modulate neuroprotection, angiogenesis, blood–brain barrier integrity and synaptic plasticity. After an ischaemic event, local and peripheral sources of these proteins counteract excitotoxicity, oxidative stress and inflammation, while promoting neurite outgrowth and vascular remodelling. Exogenous delivery or enhanced expression of specific growth factors has demonstrated infarct reduction, improved functional recovery and modulation of immune responses in animal models. Clinically, circulating levels of growth factors and their binding proteins are under investigation as prognostic biomarkers and therapeutic targets. The global significance of this research lies in the prospect of extending the treatment window beyond reperfusion and reducing long-term disability through regenerative approaches.

Research from Nature Portfolio

Neuron-derived fibroblast growth factor 10 (FGF10) was shown to accumulate in cerebrospinal fluid and is upregulated in neurons after middle cerebral artery occlusion. Intracerebroventricular administration of FGF10 reduced infarct volume and apoptotic cell death, attenuated pro-inflammatory cytokine release by suppressing NF-κB signalling and enhanced PI3K/Akt-dependent survival pathways. Inhibition of PI3K/Akt partially diminished neuroprotection but did not affect the anti-inflammatory action, indicating mechanistic separation between cell survival and immune modulation.

Growth Factors in Ischemic Stroke Recovery publication trend

The graph below shows the total number of articles in growth factors in ischemic stroke recovery across all publications each year (not limited to Nature Index journals).

Technical terms

Neuroinflammation: Activation of resident immune cells and release of cytokines in the brain following injury, which can be both protective and damaging.

PI3K/Akt pathway: Intracellular signalling cascade that promotes cell survival, growth and metabolism in response to growth factors.

Angiogenesis: Formation of new blood vessels from pre-existing vasculature, critical for restoring perfusion to ischaemic tissue.

Blood–brain barrier (BBB): Endothelial cell layer and associated structures that tightly regulate the passage of cells and molecules between blood and brain.

Sphingosine-1-phosphate receptor 1 (S1P1): G-protein-coupled receptor involved in endothelial cell migration and vascular stability during reparative angiogenesis.

References

1. Serum IGFBP-1 Concentration as a Predictor of Outcome after Ischemic Stroke—A Prospective Observational Study. International Journal of Molecular Sciences (2023).
2. Neuron-derived FGF10 ameliorates cerebral ischemia injury via inhibiting NF-κB-dependent neuroinflammation and activating PI3K/Akt survival signaling pathway in mice. Scientific Reports (2016).
3. Non-Mitogenic Fibroblast Growth Factor 1 Enhanced Angiogenesis Following Ischemic Stroke by Regulating the Sphingosine-1-Phosphate 1 Pathway. Frontiers in Pharmacology (2020).
4. Plasma levels of BDNF and EGF are reduced in acute stroke patients. Heliyon (2022).