What are the latest findings on heart disease and the gut-heart-brain-immune system axis? Transgenic mice exposed to gamma ray bursts have a genetic predisposition to heart disease. (Kim M. et al., Lancet Clin., n. 10, 12001, May 2012.) During the 18th-20th century, the importance of brain and gut-brain-immune system was often pointed to to neurodevelopmental causes. In the 1920s, the advent of gene therapy for the treatment of Alzheimer’s disease was provided with the aim of avoiding the brain—mainly liver—from causing pathology. This experiment was initially carried out in males with abnormal brains which then emerged in the 1930s, after the earliest form of brain injury had been associated with microalbuminuria. In its mid-1960s, the problem was addressed—the existence of a genotype-specific population who would make it possible to control brain-brain-immune-system for a few decades without the need for major medications. In today’s clinical environment, many people suffer from a number of health problems. A great many of them are associated with two groups of diseases: stroke, heart diseases and type 2 diabetes. According to the World Health Organization, stroke and diabetes are the causative disorders. Stroke disease mostly affects children. Heart disease can cause small losses. Stroke affects approximately 150 million people worldwide a year. By 2010 the risk of developing heart disease was estimated around 2.5 times as high. Heart is a type of disease which has been associated with many other disease conditions such as malignancy, type 2 diabetes or cancer. This makes it very difficult for heart-related damage to occur.
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In addition to heart, the gut also controls the immune system. Gut is a specialized organ that controls the immune system, it’s central function to the human organism and acts as a reservoir for other functions, like the production of immunity. It is here that the gut-brain-immune system protects individuals from diseases such as heart disease and cancer. What are the latest findings on heart disease and the gut-heart-brain-immune system axis? Among the recent studies \[[@CR5], [@CR6], [@CR13], [@CR14], [@CR17]\] it has been well established that inflammatory bowel disease, cardiometabolic syndrome and autoimmune diseases account for approximately 25 % of the human risk for heart disease \[[@CR3], [@CR5], [@CR6], [@CR19]\] and can contribute to many cardiovascular system disorders including cardiovascular and neurodegenerative disease \[[@CR13], [@CR17]\]. Risk factors include age, depression, obesity, and presence of diabetes mellitus \[[@CR3], [@CR17], [@CR19]\]. Furthermore, cardiovascular and immune dysregulation including inflammation and increased production of pro-inflammatory lipids can in turn contribute to increased total mortality in the general population \[[@CR17]\]. More importantly, cardiometabolic syndrome is a risk factor for atrial and ventricular premature labor \[[@CR20]\] where up to 20 % of male passengers with cardiometabolic syndrome die from the event in developing countries. In this context, it is important to monitor heart failure, chronic heart failure, and major surgical arrhythmias of the heart \[[@CR1], [@CR5], [@CR16], [@CR17]\] especially in developing countries and on waiting lists. Since the first successful genome-wide association study of genes on the basis of low risk and/or increased genetic risk \[[@CR2], [@CR3]\] between heart risk factors and subsequent mortality in adult patients with heart failure (HF), cardiovascular and immune complications, many efforts have been made to assess the genetic contribution of the cardiac biomarkers of the risk for the development of HF. The information, mostly from basic and clinical studies, has led to the generation of the most important information on theWhat are the latest findings on heart disease and the gut-heart-brain-immune system axis? Is the pathway shifting toward dysfunctional myocardium based on upregulation of genes related to homeostasis of immune cells, especially myeloid committed cells? The gut-heart-blood-heart role relates to several pathways that connect to gut-heart metabolism and stress signaling in the colon. The homeostatic defense, or gut-heart’s anti-inflammatory path, is important for maintaining gut-heart balance. However, not all myeloid myeloid cells play a role in limiting stress-induced inflammation. The recent report by co-workers also points out important link dysregulation of M2 macrophages and myeloid derived suppressor 1/2 (MSF-1/2) signaling are involved in gut-heart-derived immunoregulatory pathway and contributes to maintaining inducible inflammation. Research by co-workers in our laboratory further shows that in B lymphocytes, the M1 macrophage marker B220/CD40 increases in response to transient intestinal inflammation. This suggests the active role of B220 and/or M1 macrophage-cell co-receptors at the microflora level or the homeostasis of inflammatory response. However conversely, the M2 macrophage-cell co-receptors are absent from stromal cells, the latter of T-lymphocytes which are activated in response to ischemia that is associated their website an exaggerated stress response on the intestinal mucosa. In addition to M1 macrophage actin and actin-actin (MFA), M2 macrophage genes are responsible for maintaining gut-body health. While M1 macrophages are important for normal functioning of the intestinal mucosa, the role of both M2 macrophages and M1 macrophages in the gut-heart-brain metabolism remains unknown. Moreover, the mechanism of M1 macrophage function and stress-induced changes in T-cell function of the intestinal mucosa
