TY - JOUR
T1 - Preclinical and clinical research on inflammation after intracerebral hemorrhage
AU - Wang, Jian
N1 - Funding Information:
This work was supported by an American Heart Association 09BGIA2080137 and NIH K01AG031926 . I thank Claire Levine for her assistance in preparing this manuscript. The author reports no conflicts of interest.
PY - 2010/12
Y1 - 2010/12
N2 - Intracerebral hemorrhage (ICH) is one of the most lethal stroke subtypes. Despite the high morbidity and mortality associated with ICH, its pathophysiology has not been investigated as well as that of ischemic stroke. Available evidence from preclinical and clinical studies suggests that inflammatory mechanisms are involved in the progression of ICH-induced secondary brain injury. For example, in preclinical ICH models, microglial activation has been shown to occur within 1 h, much earlier than neutrophil infiltration. Recent advances in our understanding of neuroinflammatory pathways have revealed several new molecular targets, and related therapeutic strategies have been tested in preclinical ICH models. This review summarizes recent progress made in preclinical models of ICH, surveys preclinical and clinical studies of inflammatory cells (leukocytes, macrophages, microglia, and astrocytes) and inflammatory mediators (matrix metalloproteinases, nuclear factor erythroid 2-related factor 2, heme oxygenase, and iron), and highlights the emerging areas of therapeutic promise.
AB - Intracerebral hemorrhage (ICH) is one of the most lethal stroke subtypes. Despite the high morbidity and mortality associated with ICH, its pathophysiology has not been investigated as well as that of ischemic stroke. Available evidence from preclinical and clinical studies suggests that inflammatory mechanisms are involved in the progression of ICH-induced secondary brain injury. For example, in preclinical ICH models, microglial activation has been shown to occur within 1 h, much earlier than neutrophil infiltration. Recent advances in our understanding of neuroinflammatory pathways have revealed several new molecular targets, and related therapeutic strategies have been tested in preclinical ICH models. This review summarizes recent progress made in preclinical models of ICH, surveys preclinical and clinical studies of inflammatory cells (leukocytes, macrophages, microglia, and astrocytes) and inflammatory mediators (matrix metalloproteinases, nuclear factor erythroid 2-related factor 2, heme oxygenase, and iron), and highlights the emerging areas of therapeutic promise.
KW - Heme oxygenase
KW - Hemorrhagic stroke
KW - Iron
KW - Leukocytes
KW - Matrix Metalloproteinase
KW - Microglia
KW - NF-E2-related factor 2
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U2 - 10.1016/j.pneurobio.2010.08.001
DO - 10.1016/j.pneurobio.2010.08.001
M3 - Review article
C2 - 20713126
AN - SCOPUS:77956545744
SN - 0301-0082
VL - 92
SP - 463
EP - 477
JO - Progress in Neurobiology
JF - Progress in Neurobiology
IS - 4
ER -