Targeting the NF-κB pathway for therapy of ischemic stroke.
John Aaron HowellGene L BidwellPublished in: Therapeutic delivery (2020)
Ischemic strokes occur when a major cerebral artery or its branches are occluded, resulting in activation of inflammatory processes that cause secondary tissue injury, breakdown of the blood-brain barrier, edema or hemorrhage. Treatments that inhibit inflammatory processes may thus be highly beneficial. A key regulator of the inflammatory process is the nuclear factor kappa B (NF-κB) pathway. In its active form, NF-κB regulates expression of proinflammatory and proapoptotic genes. The molecules that interact with NF-κB, and the subunits that compose NF-κB itself, represent therapeutic targets that can be modulated to decrease inflammation. This review focuses on our current understanding of the NF-κB pathway and the potential benefits of inhibiting NF-κB in ischemia-reperfusion injury of the brain.
Keyphrases
- nuclear factor
- signaling pathway
- oxidative stress
- lps induced
- toll like receptor
- pi k akt
- ischemia reperfusion injury
- inflammatory response
- transcription factor
- poor prognosis
- stem cells
- cell proliferation
- atrial fibrillation
- immune response
- drug delivery
- genome wide
- risk assessment
- cerebral ischemia
- climate change
- mesenchymal stem cells