Chronic inflammation and apoptosis propagate in ischemic cerebellum and heart of non-human primates

Acosta, Sandra; Mashkouri, Sherwin; Nwokoye, Diana; Lee, Jea Y.; Borlongan, Cesar V.

doi:10.18632/oncotarget.18330

Cited by 20 publications

(9 citation statements)

References 93 publications

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“…Neural and cardiac myocyte cell death has been recently explored in other experimental settings, suggesting a potential correlation between post-AIS inflammation and cardiac dysfunction [26]. Chronic inflammation and apoptosis were found in the cerebellum and heart of non-human primates 6 months after transient global ischemia induction [27].…”

Section: The Local and Systemic Inflammatory Response To Ischemic Strokementioning

confidence: 99%

Brain–heart interaction after acute ischemic stroke

et al. 2020

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Early detection of cardiovascular dysfunctions directly caused by acute ischemic stroke (AIS) has become paramount. Researchers now generally agree on the existence of a bidirectional interaction between the brain and the heart. In support of this theory, AIS patients are extremely vulnerable to severe cardiac complications. Sympathetic hyperactivity, hypothalamic-pituitary-adrenal axis, the immune and inflammatory responses, and gut dysbiosis have been identified as the main pathological mechanisms involved in brain-heart axis dysregulation after AIS. Moreover, evidence has confirmed that the main causes of mortality after AIS include heart attack, congestive heart failure, hemodynamic instability, left ventricular systolic dysfunction, diastolic dysfunction, arrhythmias, electrocardiographic anomalies, and cardiac arrest, all of which are more or less associated with poor outcomes and death. Therefore, intensive care unit admission with continuous hemodynamic monitoring has been proposed as the standard of care for AIS patients at high risk for developing cardiovascular complications. Recent trials have also investigated possible therapies to prevent secondary cardiovascular accidents after AIS. Labetalol, nicardipine, and nitroprusside have been recommended for the control of hypertension during AIS, while beta blockers have been suggested both for preventing chronic remodeling and for treating arrhythmias. Additionally, electrolytic imbalances should be considered, and abnormal rhythms must be treated. Nevertheless, therapeutic targets remain challenging, and further investigations might be essential to complete this complex multi-disciplinary puzzle. This review aims to highlight the pathophysiological mechanisms implicated in the interaction between the brain and the heart and their clinical consequences in AIS patients, as well as to provide specific recommendations for cardiovascular management after AIS.

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Section: The Local and Systemic Inflammatory Response To Ischemic Strokementioning

confidence: 99%

Brain–heart interaction after acute ischemic stroke

et al. 2020

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“…Leukocyte-endothelial cell adhesion and platelet aggregation are mediating microthrombi and microvascular dysfunction, cardiomyocyte dysfunction, edema, and eventually cell death (84). Importantly, the increased monocytes and macrophages have been found in cardiac tissue after IS, which boost cardiac inflammation and hence promotes cardiac damage (49,63). Inhibiting inflammatory responses have been proven as an effective way to attenuate cardiac damage in CCS (11,49,52).…”

Section: Immune Response and Systemic Inflammationmentioning

confidence: 99%

Cerebral-Cardiac Syndrome and Diabetes: Cardiac Damage After Ischemic Stroke in Diabetic State

Lin

Zhang

et al. 2021

Front. Immunol.

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Cerebral-cardiac syndrome (CCS) refers to cardiac dysfunction following varying brain injuries. Ischemic stroke is strongly evidenced to induce CCS characterizing as arrhythmia, myocardial damage, and heart failure. CCS is attributed to be the second leading cause of death in the post-stroke stage; however, the responsible mechanisms are obscure. Studies indicated the possible mechanisms including insular cortex injury, autonomic imbalance, catecholamine surge, immune response, and systemic inflammation. Of note, the characteristics of the stroke population reveal a common comorbidity with diabetes. The close and causative correlation of diabetes and stroke directs the involvement of diabetes in CCS. Nevertheless, the role of diabetes and its corresponding molecular mechanisms in CCS have not been clarified. Here we conclude the features of CCS and the potential role of diabetes in CCS. Diabetes drives establish a “primed” inflammatory microenvironment and further induces severe systemic inflammation after stroke. The boosted inflammation is suspected to provoke cardiac pathological changes and hence exacerbate CCS. Importantly, as the key element of inflammation, NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome is indicated to play an important role in diabetes, stroke, and the sequential CCS. Overall, we characterize the corresponding role of diabetes in CCS and speculate a link of NLRP3 inflammasome between them.

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“…Other studies have suggested that ischemic stroke induces arrhythmia by impairing calcium and other ionic currents in ventricular cardiomyocytes [13][14][15]. Pro-inflammatory factors [16] and chronic inflammation [17] might also be involved in the cardiac dysfunction induced after ischemic stroke. An important component of inflammation, the NLR family pyrin domaincontaining 3 (NLRP3) inflammasome, has been attested to participate in many inflammatory diseases including type 2 diabetes mellitus, atherosclerosis, cardiovascular diseases, and neurodegenerative diseases [18][19][20][21][22].…”

Section: Introductionmentioning

confidence: 97%

Macrophage–NLRP3 Inflammasome Activation Exacerbates Cardiac Dysfunction after Ischemic Stroke in a Mouse Model of Diabetes

Lin

Wei

et al. 2020

Neurosci. Bull.

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Ischemic stroke is one of the leading causes of death worldwide. In the post-stroke stage, cardiac dysfunction is common and is known as the brain-heart interaction. Diabetes mellitus worsens the post-stroke outcome. Stroke-induced systemic inflammation is the major causative factor for the sequential complications, but the mechanism underlying the brain-heart interaction in diabetes has not been clarified. The NLRP3 (NLR pyrin domain-containing 3) inflammasome, an important component of the inflammation after stroke, is mainly activated in M1-polarized macrophages. In this study, we found that the cardiac dysfunction induced by ischemic stroke is more severe in a mouse model of type 2 diabetes. Meanwhile, M1-polarized macrophage infiltration and NLRP3 inflammasome activation increased in the cardiac ventricle after diabetic stroke. Importantly, the NLRP3 inflammasome inhibitor CY-09 restored cardiac function, indicating that the M1-polarized macrophage-NLRP3 inflammasome activation is a pathway underlying the brain-heart interaction after diabetic stroke.Keywords Ischemic stroke Á Diabetes mellitus Á Cardiac dysfunction Á NLRP3 inflammasome Á Macrophage Hong-Bin Lin and Guan-Shan Wei have contributed equally to this work.

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Chronic inflammation and apoptosis propagate in ischemic cerebellum and heart of non-human primates

Cited by 20 publications

References 93 publications

Brain–heart interaction after acute ischemic stroke

Brain–heart interaction after acute ischemic stroke

Cerebral-Cardiac Syndrome and Diabetes: Cardiac Damage After Ischemic Stroke in Diabetic State

Macrophage–NLRP3 Inflammasome Activation Exacerbates Cardiac Dysfunction after Ischemic Stroke in a Mouse Model of Diabetes

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