Abstract
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.
Highlights
Cerebral ischemic disease, a common form of stroke, remains one of the leading causes of morbidity and mortality worldwide
The event of cerebral ischemia likely triggers a multifaceted cascade of metabolic and biochemical events through metabolic changes caused by brain damage as detected in clinical samples and animal models [13,14,65]
In metabolic analyses involving patients, discrepancies have been observed in patterns of up- or downregulation of metabolites due to limitations in standardizing disease severity, onset time, race, diet, age, and other patient characteristics
Summary
A common form of stroke, remains one of the leading causes of morbidity and mortality worldwide. Cerebral ischemia is the fifth leading cause of death and disability impacting one million Americans every year [1]. It is caused by blockage of a blood vessel due to a thrombus or embolus [2]. Cells 2020, 9, 1630 understanding the pathological mechanisms and metabolic biomarkers of cerebral ischemia have been pursued using patient samples, animal models, and in vitro experiments [3,4,5,6,7,8,9,10,11,12,13,14,15]. We summarize the metabolic changes and biomarkers in patients with cerebral ischemia, and in in vivo and in vitro models
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