Skip to main content
Fig. 1 | Critical Care

Fig. 1

From: Modulation of mitochondrial function with near-infrared light reduces brain injury in a translational model of cardiac arrest

Fig. 1

Mechanism of ischemia–reperfusion injury and NIR-mediated neuroprotection. A Under normal conditions, complex I (CI) and complex II (CII) transfer electrons (from NADH and FADH2, respectively) through complex III (CIII) to cytochrome c oxidase (COX), where oxygen is reduced to water. Energy from the electron transfer is used to pump protons from the matrix into the intermembrane space, generating the mitochondrial membrane potential (ΔΨm). Complex V (CV) then uses this electrochemical gradient to generate ATP. B During ischemia, oxygen and electron donors are depleted and the ΔΨm collapses. Regulatory mechanisms function to maintain the ΔΨm by activating the respiratory complexes. Without oxygen, the ΔΨm cannot be restored resulting in a hyperactivated, yet inactive, respiratory chain. C During reperfusion, oxygen allows respiration to resume and increased activity of the respiratory chain during reperfusion leads to hyperpolarization of the ΔΨm and reactive oxygen species (ROS) generation. D Intervention by noninvasive modulation of COX limits hyperactivity of the respiratory chain and prevents hyperpolarization of the ΔΨm. This allows the respiratory chain to gradually return to a normal activation state without hyperpolarizing the ΔΨm. Figure generated with BioRender.com

Back to article page

Critical Care

ISSN: 1364-8535