TY - JOUR
T1 - The Role of Oxidative Stress in the Progression of Secondary Brain Injury Following Germinal Matrix Hemorrhage
AU - Nour Eldine, Mariam
AU - Alhousseini, Maryam
AU - Nour-Eldine, Wared
AU - Noureldine, Hussein
AU - Vakharia, Kunal V.
AU - Krafft, Paul R.
AU - Noureldine, Mohammad Hassan A.
N1 - Publisher Copyright:
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023.
PY - 2024/6
Y1 - 2024/6
N2 - Germinal matrix hemorrhage (GMH) can be a fatal condition responsible for the death of 1.7% of all neonates in the USA. The majority of GMH survivors develop long-term sequalae with debilitating comorbidities. Higher grade GMH is associated with higher mortality rates and higher prevalence of comorbidities. The pathophysiology of GMH can be broken down into two main titles: faulty hemodynamic autoregulation and structural weakness at the level of tissues and cells. Prematurity is the most significant risk factor for GMH, and it predisposes to both major pathophysiological mechanisms of the condition. Secondary brain injury is an important determinant of survival and comorbidities following GMH. Mechanisms of brain injury secondary to GMH include apoptosis, necrosis, neuroinflammation, and oxidative stress. This review will have a special focus on the mechanisms of oxidative stress following GMH, including but not limited to inflammation, mitochondrial reactive oxygen species, glutamate toxicity, and hemoglobin metabolic products. In addition, this review will explore treatment options of GMH, especially targeted therapy.
AB - Germinal matrix hemorrhage (GMH) can be a fatal condition responsible for the death of 1.7% of all neonates in the USA. The majority of GMH survivors develop long-term sequalae with debilitating comorbidities. Higher grade GMH is associated with higher mortality rates and higher prevalence of comorbidities. The pathophysiology of GMH can be broken down into two main titles: faulty hemodynamic autoregulation and structural weakness at the level of tissues and cells. Prematurity is the most significant risk factor for GMH, and it predisposes to both major pathophysiological mechanisms of the condition. Secondary brain injury is an important determinant of survival and comorbidities following GMH. Mechanisms of brain injury secondary to GMH include apoptosis, necrosis, neuroinflammation, and oxidative stress. This review will have a special focus on the mechanisms of oxidative stress following GMH, including but not limited to inflammation, mitochondrial reactive oxygen species, glutamate toxicity, and hemoglobin metabolic products. In addition, this review will explore treatment options of GMH, especially targeted therapy.
KW - Apoptosis
KW - Germinal matrix hemorrhage
KW - Glutamate toxicity
KW - Inflammation
KW - Iron toxicity
KW - Melatonin
KW - Oxidative stress
KW - Reactive oxygen species
KW - Therapeutic hypothermia
UR - https://www.scopus.com/pages/publications/85150153172
U2 - 10.1007/s12975-023-01147-3
DO - 10.1007/s12975-023-01147-3
M3 - Review article
C2 - 36930383
AN - SCOPUS:85150153172
SN - 1868-4483
VL - 15
SP - 647
EP - 658
JO - Translational Stroke Research
JF - Translational Stroke Research
IS - 3
ER -