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The Regulated Cell Death and Potential Interventions in Preterm Infants after Intracerebral Hemorrhage
Yanan Wu1, Yanyan Sun2, Xiaoyang Wang1,3
1Henan Key Laboratory of Child Brain Injury and Henan Pediatric Clinical Research Center, Third Affiliated Hospital and Institute of Neuroscience of Zhengzhou University, Zhengzhou 450052, China.
Insights
Intracerebral hemorrhage (ICH) in preterm infants causes neurodevelopmental deficits. This review explores regulated cell death pathways and potential interventions to protect the immature brain from secondary injury.
Area of Science:
- Neonatal neurology
- Neurobiology of cell death
- Pediatric neurosurgery
Background:
- Intracerebral hemorrhage (ICH) is a significant comorbidity in preterm infants, leading to long-term neurodevelopmental impairments.
- Current therapeutic options for preventing ICH or managing its neurological consequences in neonates are limited.
- Emerging research on regulated cell death (RCD) offers new insights into secondary brain injury mechanisms.
Approach:
- This review synthesizes current evidence on various RCD pathways implicated in preterm infant ICH.
- It examines apoptosis, necroptosis, pyroptosis, ferroptosis, autophagy, and PANoptosis in the context of neonatal brain injury.
- Potential therapeutic strategies targeting RCD pathways for neuroprotection are discussed.
Key Points:
- RCD pathways, including apoptosis and ferroptosis, play a critical role in secondary brain injury following ICH in preterm infants.
- Understanding these distinct cell death mechanisms is crucial for developing targeted interventions.
- Specific RCD pathways present viable targets for novel therapeutic strategies.
Conclusions:
- Targeting RCD pathways offers promising therapeutic avenues to mitigate secondary brain injury after ICH in preterm infants.
- Further research into these pathways may lead to effective treatments for neurodevelopmental deficits associated with neonatal ICH.
Abstract:
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.
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