Metabolic Reprogramming of Microglia in Sepsis-associated Encephalopathy: Insights from
Neuroinflammation



Sepsis-associated encephalopathy (SAE) is a diffuse brain
dysfunction caused by sepsis that manifests as a range of brain dysfunctions
from delirium to coma. It is a relatively common complication of sepsis
associated with poor patient prognosis and mortality. The pathogenesis of
SAE involves neuroinflammatory responses, neurotransmitter dysfunction,
blood-brain barrier (BBB) disruption, abnormal blood flow regulation, etc.
Neuroinflammation caused by hyperactivation of microglia is considered to
be a key factor in disease development, which can cause a series of chain
reactions, including BBB disruption and oxidative stress. Metabolic
reprogramming has been found to play a central role in microglial activation
and executive functions. In this review, we describe the pivotal role of
energy metabolism in microglial activation and functional execution and
demonstrate that the regulation of microglial metabolic reprogramming
might be crucial in the development of clinical therapeutics for
neuroinflammatory diseases like SAE.
