Metabolome Changes in Cerebral Ischemia

• Published in: Cells (Basel, Switzerland) Switzerland), 2020-07, Vol.9 (7), p.1630
• Main Authors: Shin, Tae Hwan, Lee, Da Yeon, Basith, Shaherin, Manavalan, Balachandran, Paik, Man Jeong, Rybinnik, Igor, Mouradian, M Maral, Ahn, Jung Hwan, Lee, Gwang
• Format: Article
• Language: English
• Subjects: Animals; Bioinformatics; Biomarkers; Blood flow; Brain damage; Brain injury; Brain Ischemia - genetics; Brain Ischemia - metabolism; Catheters; Cell death; Cerebral blood flow; Cerebral infarction; cerebral ischemia; Chromatography; Humans; Infarction, Middle Cerebral Artery - genetics; Infarction, Middle Cerebral Artery - metabolism; Ischemia; Magnetic resonance imaging; Medical imaging; metabolic network; Metabolism; Metabolites; Metabolome - genetics; Metabolome - physiology; metabolomics; Metabolomics - methods; MicroRNAs; middle cerebral artery occlusion; miRNA; Morbidity; NMR; Nuclear magnetic resonance; Organic acids; oxygen-glucose deprivation; Principal components analysis; Proteins; Review; Statistical analysis; Stroke; Studies; Variables; Variance analysis
• ISSN: 2073-4409; 2073-4409
• DOI: 10.3390/cells9071630

Cerebral ischemia is caused by perturbations in blood flow to the brain that trigger sequential and complex metabolic and cellular pathologies. This leads to brain tissue damage, including neuronal cell death and cerebral infarction, manifesting clinically as ischemic stroke, which is the cause of considerable morbidity and mortality worldwide. To analyze the underlying biological mechanisms and identify potential biomarkers of ischemic stroke, various in vitro and in vivo experimental models have been established investigating different molecular aspects, such as genes, microRNAs, and proteins. Yet, the metabolic and cellular pathologies of ischemic brain injury remain not fully elucidated, and the relationships among various pathological mechanisms are difficult to establish due to the heterogeneity and complexity of the disease. Metabolome-based techniques can provide clues about the cellular pathologic status of a condition as metabolic disturbances can represent an endpoint in biological phenomena. A number of investigations have analyzed metabolic changes in samples from cerebral ischemia patients and from various in vivo and in vitro models. We previously analyzed levels of amino acids and organic acids, as well as polyamine distribution in an in vivo rat model, and identified relationships between metabolic changes and cellular functions through bioinformatics tools. This review focuses on the metabolic and cellular changes in cerebral ischemia that offer a deeper understanding of the pathology underlying ischemic strokes and contribute to the development of new diagnostic and therapeutic approaches.