Unlocking extracellular mitochondria from bench to clinical application in stroke

TL;DR

Extracellular mitochondria may help protect brain cells and could be used as biomarkers or treatments for stroke.

Contribution

This review highlights recent advances in extracellular mitochondria's roles and potential clinical applications in stroke.

Findings

Extracellular mitochondria can be taken up by neurons and offer neuroprotection.

Damaged mitochondria contribute to neurodegeneration during CNS injury.

Mitochondria transplantation shows promise as a therapy for CNS disorders.

Abstract

Within the central nervous system (CNS), mitochondria serve as vital energy sources for neurons, glial cells, and vascular functions, maintaining intracellular metabolic balance. Recent studies involving cellular models, rodents, and humans reveal that metabolically active mitochondria can be released into the extracellular space, playing roles in intercellular communication within the CNS. When taken up by neurons, these extracellular mitochondria may provide neuroprotective effects. Conversely, damaged mitochondria and their released components during severe tissue injury or inflammation can contribute to neurodegenerative processes. Thus, mitochondria secreted under pathological conditions in the CNS hold promise as biomarkers indicative of recovery. Additionally, transplantation of external mitochondria shows potential as a therapeutic approach for various CNS disorders. This mini review focuses on recent advances in the transfer of mitochondria between cells, the use of extracellular mitochondria as biomarkers, and the prospects of mitochondria transplantation from experimental research to clinical application, particularly in diseases like stroke.