Medical Studies on Melatonin – Cardiovascular System
Melatonin plays a key role in cardiovascular health, for example in relation to arteriosclerosis, high blood pressure, coronary heart disease and heart attacks. This hormone has also proven to be a promising treatment method for stroke.
Melatonin as a blood pressure regulator
High blood pressure and the constriction of the blood vessels that this entails may have fatal consequences if the key organs are no longer sufficiently supplied with blood and can therefore no longer be supplied with enough oxygen. The result is a substantial increase in the risk of heart attack or stroke. Studies have demonstrated that melatonin reduces both blood pressure and vascular stiffness and therefore has very positive effects on cardiovascular health.
Melatonin reduces cell damage
Thanks to its highly anti-oxidative and anti-inflammatory properties, melatonin can also significantly reduce the extent of cell damage that often occurs after a heart attack or stroke. Free radicals in particular can affect the severity of these medical emergencies, because the tissue damage that they cause is irreparable.
Protection from dangerous oxidative stress
Melatonin has proven to be highly efficient both in preventing and treating acute diseases. It protects against oxidative stress and establishes a balance between pro-inflammatory and anti-inflammatory cytokines, and can, for example, in the event of a heart attack, even protect the heart from injury after myocardial ischaemia or during essential reperfusion.
Medical Studies on Melatonin – Cardiovascular System
Role of melatonin in the angiogenesis potential; highlights on the cardiovascular disease
Melatonin possesses multi-organ and pleiotropic effects with potency to control angiogenesis at both molecular and cellular levels. To date, many efforts have been made to control and regulate the dynamic of angiogenesis modulators in a different milieu.
Melatonin, cardiovascular disease and COVID-19: A potential therapeutic strategy?
The mechanism for SARS-CoV-2 infection is the requisite binding of the virus to the membrane-bound form of angiotensin-converting enzyme 2 (ACE2) and internalization of the complex by the host cell. SARS-CoV-2 induced endothelial dysfunction and cardiovascular injury are probably initiated by increases in the phosphorylation levels of JAK2 and STAT3 and resultant reactive oxygen species (ROS) formation. These pathological alterations are speculated to be strikingly reversed by melatonin.
The Effects of Melatonin Supplementation on Parameters of Mental Health, Glycemic Control, Markers of Cardiometabolic Risk, and Oxidative Stress in Diabetic Hemodialysis Patients: A Randomized, Double-Blind, Placebo-Controlled Trial.
This study evaluated the effects of melatonin supplementation on parameters of mental health, glycemic control, markers of cardiometabolic risk, and oxidative stress in diabetic hemodialysis (HD) patients.
Melatonin alleviates cardiac fibrosis via inhibiting lncRNA MALAT1/miR-141-mediated NLRP3 inflammasome and TGF-β1/Smads signaling in diabetic cardiomyopathy.
Melatonin is a hormone produced by the pineal gland, and it has extensive beneficial effects on various tissue and organs; however, whether melatonin has any effect on cardiac fibrosis in the pathogenesis of diabetic cardiomyopathy (DCM) is still unknown.
Poor sleep quality associates with self-reported psychiatric and cardiometabolic symptoms independently of sleep timing patterns in a large sample of rural and urban workers.
Poor sleep associates with mental and cardiometabolic pathological outcomes. The participation of sleep timing features in the pathways by which this relationship occurs is not clear.
Melatonin has profound effects on mitochondrial dynamics in myocardial ischaemia/reperfusion.
Research focus recently shifted to mitochondrial dynamics and the role of fusion and fission in cardioprotection. The aim of this study was to evaluate (i) the function and dynamics of mitochondria isolated from hearts exposed to ischaemia/reperfusion (I/R) (ii) the effects of melatonin, a powerful cardioprotectant, on mitochondrial dynamics in I/R.
Infusion of Melatonin Into the Paraventricular Nucleus Ameliorates Myocardial Ischemia-Reperfusion Injury by Regulating Oxidative Stress and Inflammatory Cytokines.
Melatonin, the receptors for which are abundant in the hypothalamic paraventricular nucleus (PVN), can protect the heart from myocardial ischemia-reperfusion (MI/R) injury. The aim of this study was to determine whether the infusion of melatonin into the PVN protects the heart from MI/R injury by suppressing oxidative stress or regulating the balance between proinflammatory cytokines and anti-inflammatory cytokines in MI/R rats.
Cardioprotective Melatonin: Translating from Proof-of-Concept Studies to Therapeutic Use.
In this review we summarized the actual clinical data for a cardioprotective therapeutic role of melatonin, listed melatonin and its agonists in different stages of development, and evaluated the melatonin cardiovascular target tractability and prediction using machine learning on ChEMBL.
Melatonin protects circulatory death heart from ischemia/reperfusion injury via the JAK2/STAT3 signalling pathway.
The shortage of donor hearts could be alleviated with the use of the allografts from donation after circulatory death (DCD). Here, we evaluated the protective effect of melatonin on myocardial ischemia/reperfusion (MI/R) injury in a DCD heart model after ex vivo perfusion.
Melatonin: Countering Chaotic Time Cues.
Last year melatonin was 60 years old, or at least its discovery was 60 years ago. The molecule itself may well be almost as old as life itself. So it is time to take yet another perspective on our understanding of its functions, effects and clinical uses.
Melatonin in Heart Failure: A Promising Therapeutic Strategy?
Heart failure is a multifactorial clinical syndrome characterized by the inability of the heart to pump sufficient blood to the body. Despite recent advances in medical management, poor outcomes in patients with heart failure remain very high. This highlights a need for novel paradigms for effective, preventive and curative strategies.
Melatonin as an antioxidant: under promises but over delivers.
Melatonin is uncommonly effective in reducing oxidative stress under a remarkably large number of circumstances. It achieves this action via a variety of means: direct detoxification of reactive oxygen and reactive nitrogen species and indirectly by stimulating antioxidant enzymes while suppressing the activity of pro-oxidant enzymes.
Melatonin in bacterial and viral infections with focus on sepsis: a review.
Melatonin is a versatile molecule, synthesized not only by the pineal gland, but also in small amounts by many other organs like retina, gastrointestinal tract, thymus, bone marrow, lymphocytes etc.
Melatonin: action as antioxidant and potential applications in human disease and aging.
This review aims at describing the beneficial properties of melatonin related to its antioxidant effects. Oxidative stress, i.e., an imbalance between the production of reactive oxygen species and antioxidant defences, is involved in several pathological conditions such as cardiovascular or neurological disease, and in aging. Therefore, research for antioxidants has developed. However, classical antioxidants often failed to exhibit beneficial effects, especially in metabolic diseases.
Beneficial effects of melatonin in cardiovascular disease.
The experimental data obtained from both human and rodent studies suggest that melatonin may have utility in the treatment of several cardiovascular conditions. In particular, melatonin's use in reducing the severity of essential hypertension should be more widely considered. In rodent studies melatonin has been shown to be highly effective in limiting abnormal cardiac physiology and the loss of critical heart tissue resulting from ischemia/reperfusion injury.
Melatonin ameliorates neurologic damage and neurophysiologic deficits in experimental models of stroke.
This review summarizes the numerous reports that have documented the neuroprotective actions of melatonin in experimental models of ischemia/reperfusion injury (stroke).
Administration of melatonin after onset of ischemia reduces the volume of cerebral infarction in a rat middle cerebral artery occlusion stroke model.
In both permanent and transient 3-hour middle cerebral artery occlusion rat stroke models, a single intraperitoneal injection of melatonin at 5 or 15 mg/kg given before ischemia was shown to reduce infarct volume at 72 hours. The present study was conducted to examine the treatment time window when melatonin was commenced after onset of ischemia.