ReviewOxidative medicine and cellular longevity2022
Biological Effects and Mechanisms of Caspases in Early Brain Injury after Subarachnoid Hemorrhage.
Review in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Protective Effect of luteolin on CLP-induced Sepsis-associated Encephalopathy via Inhibiting p38 MAPK Signalling in a Rat Model.Molecular neurobiology · 2026Article
- Mechanisms and interventions in aneurysmal subarachnoid hemorrhage: Unraveling the role of inflammatory responses and cell death in early brain injury (Review).Molecular medicine reports · 2025Review
- RNA-binding protein DAZAP1 accelerates the advancement of pancreatic cancer by inhibiting ferroptosis.European journal of medical research · 2025Article
- Mechanisms and potential therapeutic molecular targets in blood-brain barrier disruption following subarachnoid hemorrhage: a review of early brain injury.Frontiers in neurology · 2025Review
- Taurine ameliorates sensorimotor function by inhibiting apoptosis and activating A2 astrocytes in mice after subarachnoid hemorrhage.Amino acids · 2024Article
- Hyperchloremia and Hypernatremia Decreased Microglial and Neuronal Survival during Oxygen-Glucose Deprivation/Reperfusion.Biomedicines · 2024Article
- Pharmacological Inhibition of Ferroptosis as a Therapeutic Target for Neurodegenerative Diseases and Strokes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Review
- ASK1 inhibitor NQDI‑1 decreases oxidative stress and neuroapoptosis via the ASK1/p38 and JNK signaling pathway in early brain injury after subarachnoid hemorrhage in rats.Molecular medicine reports · 2023Article
- The mechanism of ferroptosis in early brain injury after subarachnoid hemorrhage.Frontiers in immunology · 2023Review
- The Role of Nursing Care in the Management of Patients with Traumatic Subarachnoid Hemorrhage.Galen medical journal · 2023Article
- Understanding Acquired Brain Injury: A Review.Biomedicines · 2022Review
- Saikosaponin D Inducing Apoptosis and Autophagy through the Activation of Endoplasmic Reticulum Stress in Glioblastoma.BioMed research international · 2022Article
- Crosstalk among N6-methyladenosine modification and RNAs in central nervous system injuries.Frontiers in cellular neuroscience · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caspases are an evolutionarily conserved family of proteases responsible for mediating and initiating cell death signals. In the past, the dysregulated activation of caspases was reported to play diverse but equally essential roles in neurodegenerative diseases, such as brain injury and neuroinflammatory diseases. A subarachnoid hemorrhage (SAH) is a traumatic event that is either immediately lethal or induces a high risk of stroke and neurological deficits. Currently, the prognosis of SAH after treatment is not ideal. Early brain injury (EBI) is considered one of the main factors contributing to the poor prognosis of SAH. The mechanisms of EBI are complex and associated with oxidative stress, neuroinflammation, blood-brain barrier disruption, and cell death. Based on mounting evidence, caspases are involved in neuronal apoptosis or death, endothelial cell apoptosis, and increased inflammatory cytokine-induced by apoptosis, pyroptosis, and necroptosis in the initial stages after SAH. Caspases can simultaneously mediate multiple death modes and regulate each other. Caspase inhibitors (including XIAP, VX-765, and Z-VAD-FMK) play an essential role in ameliorating EBI after SAH. In this review, we explore the related pathways mediated by caspases and their reciprocal regulation patterns after SAH. Furthermore, we focus on the extensive crosstalk of caspases as a potential area of research on therapeutic strategies for treating EBI after SAH.
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