PI3K/Akt pathway and neuroinflammation in sepsis-associated encephalopathy

TL;DR

This review explores how the PI3K/Akt pathway influences neuroinflammation in sepsis-associated encephalopathy and suggests it as a potential target for treatment.

Contribution

The paper systematically reviews the role of the PI3K/Akt pathway in SAE neuroinflammation and highlights new therapeutic strategies.

Findings

The PI3K/Akt pathway regulates neuroinflammation and BBB integrity in SAE.

Targeting this pathway may reduce neuroinflammation and improve neurological outcomes.

Development of pathway-specific agonists and inhibitors offers new therapeutic opportunities.

Abstract

Sepsis-associated encephalopathy (SAE) is a complex neurological complication of sepsis involving activation of microglia in the central nervous system (CNS), blood–brain barrier (BBB) dysfunction, neurotransmitter dysfunction, impaired brain metabolism, and mitochondrial dysfunction. Neuroinflammation is a critical component of the pathogenesis. The phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway, as a key intracellular signaling pathway, plays a crucial role in regulating neuroinflammation, maintaining the integrity of the BBB, and promoting neuronal cell survival.

This review aims to summarize the role of the PI3K/Akt pathway in SAE-associated neuroinflammation and highlights potential therapeutic targets and strategies for its management.

We systematically reviewed recent basic and clinical studies on PI3K/Akt signaling pathway in neuroinflammation associated with SAE, as well as the development of pathway-specific agonists and inhibitors.

The PI3K/Akt pathway serves as a crucial intracellular signaling axis involved in the regulation of neuroinflammatory processes. Accumulating evidence indicates that targeted modulation of this pathway may alleviate neuroinflammation associated with SAE and enhance neurological recovery.

Targeting the PI3K/Akt pathway represents a promising therapeutic approach for SAE. Advances in the development of specific agonists and inhibitors provide new opportunities for clinical translation and drug discovery in neuroinflammatory conditions.

Figures