The Regulated Cell Death and Potential Interventions in Preterm Infants after Intracerebral Hemorrhage

Intracerebral hemorrhage (ICH) in preterm infants is one of the major co-morbidities of preterm birth and is associated with long-term neurodevelopmental deficits. There are currently no widely accepted treatments to prevent ICH or therapies for the neurological sequelae. With studies broadening the scope of cell death, the newly defined concept of regulated cell death has enriched our understanding of the underlying mechanisms of secondary brain injury after ICH and has suggested potential interventions in preterm infants. In this review, we will summarize the current evidence for regulated cell death pathways in preterm infants after ICH, including apoptosis, necroptosis, pyroptosis, ferroptosis, autophagy, and PANoptosis as well as several potential intervention strategies that may protect the immature brain from secondary injury after ICH through regulating regulated cell death.

Automated summary

In preterm infants, intracerebral hemorrhage (ICH) is a major complication of preterm birth and is linked to long-term neurodevelopmental impairments. Currently, there are no widely accepted preventive or therapeutic measures for ICH and its neurological consequences. However, with the expanding understanding of cell death mechanisms, researchers have identified regulated cell death pathways that may offer potential interventions to protect the immature brain from secondary injury after ICH. This review summarizes the current evidence for regulated cell death pathways in preterm infants after ICH, including apoptosis, necroptosis, pyroptosis, ferroptosis, autophagy, and PANoptosis, as well as potential strategies to regulate these cell death processes for neuroprotection.