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It is clear that despite advances in pharmacy and clinical practice, heart disease remains a major public health problem. Providers can usually treat the symptoms of heart disease, but they progressively worsen until something radical is done, or worse, until something goes wrong. serious happen. Treatments for other diseases, such as an antibiotic for an ear infection, simultaneously eliminate the symptoms and get rid of the disease; but this is not often the case with heart disease. It always intrigued me. It is now well understood that one of the reasons why heart disease is so difficult to treat is that it starts well before any sign of disease can be detected. Negative forces, such as high blood pressure or smoking, can work overtime for cells and tissues. Once these cells and tissues are damaged or dysfunctional, the breeds suffer. Unfortunately, the finish line is marked by flasks of pills and visits to the doctor.
Scientists, doctors and epidemiologists have identified many of the harmful forces that cause damage to cells and cardiovascular tissue, leading to heart disease. Together, these forces are called "risk factors for cardiovascular disease". Most are known things that we have long known as being at the root of heart disease, such as smoking, cholesterol and diabetes. But a new risk factor emerges. To sleep.
Studies by scientists around the world have shown that a lack of sleep harms cardiovascular health. For example, our laboratory, the Integrative Vascular Biology Laboratory at the University of Colorado at Boulder, found that the cells lining the blood vessels help regulate blood pressure and release pertussis substances that function abnormally in adults sleeping less than the recommended seven hours a night, compared to those who sleep seven to nine hours a night1,2. Other labs have clearly shown that lack of sleep is badociated with increased atherosclerosis, or plaque development that causes heart attacks.3 But we do not understand why or how.
We recently published a study in the journal Experimental physiology examine the difference in blood levels of important physiological regulators, or microRNAs, in people who sleep less than and more than seven hours a night. We studied 24 healthy middle-aged adults (44 to 62 years old). Half of the subjects reported sleeping usually less than seven hours a night, while the other half slept regularly between seven and nine hours a night. We discovered that the circulating levels of three specific MicroRNAs (miR-125a, miR-126 and miR-146a) were significantly lower in those who slept less than seven hours per night. These three microRNAs have been shown to be powerful promoters of cardiovascular health, acting as breaks in the cellular processes leading to cardiovascular disease.
MicroRNAs are small molecules that stop the production, or "expression," of certain proteins in cells. To a certain extent, they determine overall cellular health and function by inhibiting the expression of some proteins, but not others. We found that three microRNAs were lower in people with short sleep – miR-125a, miR-12 and miR-146a. It has already been shown that they block the production of proteins that induce vascular inflammation and dysfunction.4-6 Extensive clinical studies have linked the low concentrations of these three microRNAs with the development and progression of these microRNAs. 39, heart disease7,8. a new mechanism by which sleep influences heart health and physiology. In addition, these findings suggest that there may be a "fingerprint" of insufficient night-time sleep that physicians may be able to use to badess a person's sleep health.
Does this mean that if we have a period of bad sleep, we are doomed? It is still in the air. Research is underway to determine whether restoring healthy sleep patterns in those sleeping less than seven hours per night can restore circulating microRNA levels to normal and improve the health and functioning of the cardiovascular system.
REFERENCES
1. AR Bath, Weil BR, KJ Diehl, Greiner JJ, BL Stauffer, CA DeSouza. Insufficient sleep is badociated with nitric oxide-induced endothelial-dependent vasodilatation. atherosclerosis. 2017 265: 41-46. doi: 10.1016 / j.atherosclerosis.2017.08.001.
2. Weil BR, ML Mestek, Westby CM, Van Guilder GP, Greiner JJ, BL Stauffer, CA DeSouza. A short duration of sleep is badociated with an improved vasoconstrictor tone of endothelin-1. This article is part of a selection of articles published in the two-part special issue entitled 20 Years of Endothelin Research. Can J Physiol Pharmacol. 2010; 88 (8): 777-781. Doi: 10.1139 / Y10-046.
3. Jackson CL, Redline S, Emmons KM. Sleep as a potential fundamental contributor to disparities in cardiovascular health. Annu Rev Public Health. 2015; 36: 417-440. doi: 10.1146 / annurev-publhealth-031914-122838.
4. Hao L, Wang X, Cheng J, You S, Ma S, Zhong X, Quan L and Luo B. Upregulation of endothelin-1 and downregulation of miRNA-125a 5p, -155, and – 199a / b-3p in the human atherosclerotic coronary artery. Cardiovasc Pathol. 2014; 23 (4): 217-223. doi: 10.1016 / j.carpath.2014.03.009.
5. DA Chistiakov, AN Orekhov, Bobryshev YV. The role of miR-126 in embryonic angiogenesis, vascular homeostasis in adults and vascular repair and its modifications in atherosclerosis. J Mol Cell Cardiol. 2016 97: 47-55. doi: 10.1016 / j.yjmcc.2016.05.007.
6. Kamali K, ES Korjan, Eftekhar E, Malekzadeh K, Sufi FG. The role of miR-146a on the level of NF-κB expression in endothelial cells of the human umbilical vein under conditions of hyperglycemia. Bratisl Med J. 2016 117 (07): 376-380. doi: 10.4149 / BLL_2016_074.
7. Wronska A, Kurkowska-Jastrzebska I, Santulli G. Application of microRNA to the diagnosis and treatment of cardiovascular diseases. Acta Physiol. 2015; 213 (1): 60-83. doi: 10.1111 / apha.12416.
8. Barwari T, Joshi A, Mayr M. MicroRNA in cardiovascular diseases. J Am Coll Cardiol. 2016 68 (23): 2577-2584. doi: 10.1016 / j.jacc.2016.09.945.
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