Fig. 6.

Dysregulated mitochondrial dynamics in sepsis. In prolonged sepsis, the fission-to-fusion ratio favours fission. This imbalance causes the accumulation of damaged mitochondria, oxidative stress, and cell death. Treatment with procyanidin B2 (PCB2) promotes Nrf2 translocation into the nucleus, which indirectly upregulates mitochondrial fusion while inhibiting fission [176]. Melatonin increases the activity and expression of SIRT3, which preserves mitochondrial quality control mechanisms and alleviates sepsis-induced injury [177]. This highlights the potential therapeutic benefits of targeting mitochondrial dynamics and quality control in sepsis.