Cardiovascular and Neuronal Consequences of Thyroid Hormones Alterations in the Ischemic Stroke

Abstract

Ischemic stroke is one of the leading global causes of neurological morbidity and decease. Its etiology depends on multiple events such as cardiac embolism, brain capillaries occlusion and atherosclerosis, which ultimately culminate in blood flow interruption, incurring hypoxia and nutrient deprivation. Thyroid hormones (THs) are pleiotropic modulators of several metabolic pathways, and critically influence different aspects of tissues development. The brain is a key TH target tissue and both hypo- and hyperthyroidism, during embryonic and adult life, are associated with deranged neuronal formation and cognitive functions. Accordingly, increasing pieces of evidence are drawing attention on the consistent relationship between the THs status and the acute cerebral and cardiac diseases. However, the concrete contribution of THs systemic or local alteration to the pathology outcome still needs to be fully addressed. In this review, we aim to summarize the multiple influences that THs exert on the brain and heart patho-physiology, to deepen the reasons for the harmful effects of hypo- and hyperthyroidism on these organs and to provide insights on the intricate relationship between the THs variations and the pathological alterations that take place after the ischemic injury.

Network-pharmacology-based study on the mechanism of fibrates regulating HIF-1A in the treatment of ischemic stroke

“…When IS occurs, the hypothalamic-pituitary-thyroid axis will respond to the ischemic/hypoxic environment, it will reduce the levels of T3 and FT3 and increase the levels of T4 and TSH. On the contrary, if the levels of T3 and FT3 increase and the levels of T4 and TSH decrease, it means that the patient has already enters the recovery period of IS 40 . Therefore, the thyroid hormone signaling pathway is involved in the whole pathological process of IS, the changes of thyroid hormone levels can re ect the disease state of patients, so the prevention and treatment of IS can be formulated by studying thyroid hormone levels.…”

Exploring the causal factor effects of hypothyroidism on ischemic stroke: a two-sample Mendelian randomization study

“…Given that rapid reperfusion such as, endovascular therapy (EVT) and intravenous thrombolysis, is an effective treatment for neurological injuries induced by acute ischemic stroke (AIS), timely and accurate identification of ischemic injuries is paramount for implementing acute interventions and devising strategies to prevent recurrence. Research indicates that both absolute and relative deficiencies in thyroid hormones can intensify cerebrovascular atherosclerosis, thereby influencing the prevalence and outcomes of cerebrovascular diseases (5)(6)(7). Some cross-sectional studies have identified a correlation between the concentration of thyroid-stimulating hormone (TSH) and the intensification of symptoms associated with AIS.…”