Biomaterial Database

Efferocytosis Mediated Modulation of Injury after Neonatal Brain Hypoxia-Ischemia. 2021

Jana Krystofova Mike, and Donna Marie Ferriero

Department of Pediatrics, University of California San Francisco, San Francisco, CA 94143, USA.

Neonatal brain hypoxia-ischemia (HI) is a leading cause of morbidity and long-term disabilities in children. While we have made significant progress in describing HI mechanisms, the limited therapies currently offered for HI treatment in the clinical setting stress the importance of discovering new targetable pathways. Efferocytosis is an immunoregulatory and homeostatic process of clearance of apoptotic cells (AC) and cellular debris, best described in the brain during neurodevelopment. The therapeutic potential of stimulating defective efferocytosis has been recognized in neurodegenerative diseases. In this review, we will explore the involvement of efferocytosis after a stroke and HI as a promising target for new HI therapies.

UI	MeSH Term	Description	Entries
D007231	Infant, Newborn	An infant during the first 28 days after birth.	Neonate,Newborns,Infants, Newborn,Neonates,Newborn,Newborn Infant,Newborn Infants
D008954	Models, Biological	Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.	Biological Model,Biological Models,Model, Biological,Models, Biologic,Biologic Model,Biologic Models,Model, Biologic
D001930	Brain Injuries	Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.	Brain Lacerations,Acute Brain Injuries,Brain Injuries, Acute,Brain Injuries, Focal,Focal Brain Injuries,Injuries, Acute Brain,Injuries, Brain,Acute Brain Injury,Brain Injury,Brain Injury, Acute,Brain Injury, Focal,Brain Laceration,Focal Brain Injury,Injuries, Focal Brain,Injury, Acute Brain,Injury, Brain,Injury, Focal Brain,Laceration, Brain,Lacerations, Brain
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000818	Animals	Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA.	Animal,Metazoa,Animalia
D017209	Apoptosis	A regulated cell death mechanism characterized by distinctive morphologic changes in the nucleus and cytoplasm, including the endonucleolytic cleavage of genomic DNA, at regularly spaced, internucleosomal sites, i.e., DNA FRAGMENTATION. It is genetically programmed and serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.	Apoptosis, Extrinsic Pathway,Apoptosis, Intrinsic Pathway,Caspase-Dependent Apoptosis,Classic Apoptosis,Classical Apoptosis,Programmed Cell Death,Programmed Cell Death, Type I,Apoptoses, Extrinsic Pathway,Apoptoses, Intrinsic Pathway,Apoptosis, Caspase-Dependent,Apoptosis, Classic,Apoptosis, Classical,Caspase Dependent Apoptosis,Cell Death, Programmed,Classic Apoptoses,Extrinsic Pathway Apoptoses,Extrinsic Pathway Apoptosis,Intrinsic Pathway Apoptoses,Intrinsic Pathway Apoptosis
D017628	Microglia	The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling.	Microglial Cell,Cell, Microglial,Microglial Cells,Microglias
D020521	Stroke	A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)	Apoplexy,Cerebral Stroke,Cerebrovascular Accident,Cerebrovascular Apoplexy,Vascular Accident, Brain,CVA (Cerebrovascular Accident),Cerebrovascular Accident, Acute,Cerebrovascular Stroke,Stroke, Acute,Acute Cerebrovascular Accident,Acute Cerebrovascular Accidents,Acute Stroke,Acute Strokes,Apoplexy, Cerebrovascular,Brain Vascular Accident,Brain Vascular Accidents,CVAs (Cerebrovascular Accident),Cerebral Strokes,Cerebrovascular Accidents,Cerebrovascular Accidents, Acute,Cerebrovascular Strokes,Stroke, Cerebral,Stroke, Cerebrovascular,Strokes,Strokes, Acute,Strokes, Cerebral,Strokes, Cerebrovascular,Vascular Accidents, Brain
D020925	Hypoxia-Ischemia, Brain	A disorder characterized by a reduction of oxygen in the blood combined with reduced blood flow (ISCHEMIA) to the brain from a localized obstruction of a cerebral artery or from systemic hypoperfusion. Prolonged hypoxia-ischemia is associated with ISCHEMIC ATTACK, TRANSIENT; BRAIN INFARCTION; BRAIN EDEMA; COMA; and other conditions.	Anoxia-Ischemia, Brain,Anoxia-Ischemia, Cerebral,Anoxic-Ischemic Encephalopathy,Brain Anoxia-Ischemia,Brain Hypoxia-Ischemia,Brain Ischemia-Anoxia,Brain Ischemia-Hypoxia,Cerebral Anoxia-Ischemia,Cerebral Hypoxia-Ischemia,Cerebral Ischemia-Anoxia,Cerebral Ischemia-Hypoxia,Hypoxia-Ischemia, Cerebral,Hypoxic-Ischemic Encephalopathy,Ischemia-Anoxia, Brain,Ischemia-Anoxia, Cerebral,Ischemia-Hypoxia, Brain,Ischemia-Hypoxia, Cerebral,Ischemic-Hypoxic Encephalopathy,Encephalopathy, Anoxic-Ischemic,Encephalopathy, Hypoxic-Ischemic,Anoxia Ischemia, Brain,Anoxia Ischemia, Cerebral,Anoxia-Ischemias, Brain,Anoxia-Ischemias, Cerebral,Anoxic Ischemic Encephalopathy,Anoxic-Ischemic Encephalopathies,Brain Anoxia Ischemia,Brain Anoxia-Ischemias,Brain Hypoxia Ischemia,Brain Hypoxia-Ischemias,Brain Ischemia Anoxia,Brain Ischemia Hypoxia,Brain Ischemia-Anoxias,Brain Ischemia-Hypoxias,Cerebral Anoxia Ischemia,Cerebral Anoxia-Ischemias,Cerebral Hypoxia Ischemia,Cerebral Hypoxia-Ischemias,Cerebral Ischemia Anoxia,Cerebral Ischemia Hypoxia,Cerebral Ischemia-Anoxias,Cerebral Ischemia-Hypoxias,Encephalopathies, Anoxic-Ischemic,Encephalopathies, Hypoxic-Ischemic,Encephalopathies, Ischemic-Hypoxic,Encephalopathy, Anoxic Ischemic,Encephalopathy, Hypoxic Ischemic,Encephalopathy, Ischemic-Hypoxic,Hypoxia Ischemia, Brain,Hypoxia Ischemia, Cerebral,Hypoxia-Ischemias, Brain,Hypoxia-Ischemias, Cerebral,Hypoxic Ischemic Encephalopathy,Hypoxic-Ischemic Encephalopathies,Ischemia Anoxia, Brain,Ischemia Anoxia, Cerebral,Ischemia Hypoxia, Brain,Ischemia Hypoxia, Cerebral,Ischemia-Anoxias, Brain,Ischemia-Anoxias, Cerebral,Ischemia-Hypoxias, Brain,Ischemia-Hypoxias, Cerebral,Ischemic Hypoxic Encephalopathy,Ischemic-Hypoxic Encephalopathies