Stroke leaves a great economic burden due to its high morbidity and mortality. Rapid revascularization of targeted vessel(s) is the effective treatment for ischemic stroke, but subsequent ischemia-reperfusion (I/R) injury is a common complication following revascularization, leading to microcirculation dysfunction and infarct volume increase. Thrombo-inflammation, the interaction between thrombosis and inflammation, plays a critical role in the pathophysiology of ischemic stroke. In the context of I/R injury, thrombo-inflammation consists of platelet activation, endothelial injury, and inflammatory cell infiltration. Numerous studies are devoted to exploring methods of regulating thrombo-inflammation to mitigate I/R injury post-stroke, including blocking activations of platelets and neutrophils. Drugs such as antiplatelet medications, anticoagulants, and glucocorticoids have been confirmed to have the potential to regulate thrombo-inflammation. Furthermore, several recently developed drugs have also shown promises in relieving I/R injury by manipulating thrombo-inflammation. However, the majority of these studies are still in the preclinical stage. Herein, in this review, we will address the mechanisms of thrombo-inflammation in ischemic stroke, related research advances, and particularly the clinical feasibility of thrombo-inflammation as a therapeutic strategy against I/R injury.
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http://dx.doi.org/10.1007/s12035-024-04397-w | DOI Listing |
Drug Des Devel Ther
January 2025
Department of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.
Purpose: This study aimed to assess the protective effect of a clinical dose esketamine on cerebral ischemia/reperfusion (I/R) injury and to reveal the potential mechanisms associated with microglial polarization and autophagy.
Methods: Experimental cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in adult rats and simulated by oxygen-glucose deprivation (OGD) in BV-2 microglial cells. Neurological and sensorimotor function, cerebral infarct volume, histopathological changes, mitochondrial morphological changes, and apoptosis of ischemic brain tissues were assessed in the presence or absence of esketamine and the autophagy inducer rapamycin.
World J Cardiol
January 2025
Cardiac Care Unit, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, China.
Background: Myocardial ischemia/reperfusion (I/R) injury, which is associated with high morbidity and mortality, is a main cause of unexpected myocardial injury after acute myocardial infarction. However, the underlying mechanism remains unclear. Circular RNAs (circRNAs), which are formed from protein-coding genes, can sequester microRNAs or proteins, modulate transcription and interfere with splicing.
View Article and Find Full Text PDFFood Funct
January 2025
The Affiliated Changsha Hospital of Xiangya School of Medicine, Central South University, Changsha 410000, China.
A balanced diet is essential for maintaining human health. Increasing evidence suggests that dietary and nutritional interventions contribute to disease management and are associated with reduced healthcare costs and economic burden. Ferroptosis, a novel type of regulated cell death (RCD) driven by lipid peroxidation, has been shown to be involved in various pathological conditions, including diabetes, ischemia/reperfusion (I/R) injury, inflammation-related diseases, and cancer.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
February 2025
Department of Cardiology, Affiliated Hospital of Hebei University, Baoding, China.
Ischemia-reperfusion (I/R) injury is a significant clinical problem impacting the heart and other organs, such as the kidneys and liver. This study explores the protective effects of oxycodone on myocardial I/R injury and its underlying mechanisms. Using a myocardial I/R model in Sprague-Dawley (SD) rats and an oxygen-glucose deprivation/reoxygenation (OGD/R) model in H9c2 cells, we administered oxycodone and inhibited AMP-activated protein kinase (AMPK) with Compound C (C.
View Article and Find Full Text PDFCell Death Dis
January 2025
Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, and the Department of Physiology, School of Basic Medicine, Shanxi Medical University, Taiyuan, China.
Programmed necrosis/necroptosis greatly contributes to the pathogenesis of cardiac disorders including myocardial infarction, ischemia/reperfusion (I/R) injury and heart failure. However, the fundamental mechanism underlying myocardial necroptosis, especially the mitochondria-dependent death pathway, is poorly understood. Synaptotagmin-1 (Syt1), a Ca sensor, is originally identified in nervous system and mediates synchronous neurotransmitter release.
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