Women generally live longer. According to the World Health Organization World Health Statistics 2019, the average life expectancy for women worldwide is 74.2 years, compared with 69.8 years for men , the average life expectancy of women is 4.4 years longer than that of men. In old age, men have a higher risk of death than women.
July 14, 2022, USAUniversity of Virginia, SwedenUppsala Universityresearchers at” Science ” published a A research paper titled “Hematopoietic loss of Y chromosome leads to cardiac fibrosis and heart failure mortality”.
This study sheds light on why men live shorter Loss of the Y chromosome leads to cardiac fibrosis, impaired heart function and the risk of death from cardiovascular disease, making men live shorter on average than women.
women have two chromosomes. , the male has an X and a Y. But as they age, many men lose their Y chromosomes in some of their cells, and this is more severe in smokers, a change known as mLOY. Loss of the Y chromosome occurs primarily in rapidly renewing cells, such as blood cells.
mLOY is common in older men, with mLOY occurring in 60- and 70-year-old men Around 20% and 40%. Researchers have previously observed that men who suffer Y chromosome loss are more likely to die at a young age and develop age-related diseases such as Alzheimer’s disease.
In this study, researchers used the gene editing tool CRISPR to generate a mouse model of mLOY in white blood cells, To better understand the impact of Y chromosome loss in blood.
Researchers found that mLOY caused a direct effect on the internal organs of animals damage, and the survival of mice with mLOY was shorter compared to mice without mLOY. This loss of the Y chromosome accelerates age-related disease and makes mice more prone to cardiac fibrosis, which leads to decreased cardiac function and earlier death.
Age-Related Cardiac Dysfunction
In addition, the researchers found abnormal levels of overall inflammation in mice, with A complex series of reactions goes through the immune system, leading to a process of fibrosis throughout the body. The researchers believe this tug-of-war within the immune system may accelerate disease development.
Importantly, when the researchers blocked this signaling pathway, the heart pathological changes caused by mLOY may be reversed.
In addition to smallThe researchers also confirmed a causal relationship in mice through human epidemiological studies. After three analyses of data collected in the UK Biobank database, they found that mLOY is the male heart. An important risk factor for death from vascular disease, the risk of death increases with increased chromosome loss.
Specifically, mLOY was present in the blood at the start of the study of men had an approximately 30% increased risk of dying from heart failure and other types of cardiovascular disease over approximately 11 years of follow-up.
Men with higher percentages of white blood cells containing mLOY in their blood are more likely to die from cardiovascular disease, researchers say Risk is greater. This observation is consistent with results from mouse models, suggesting that mLOY also has direct physiological effects in humans.
A potential treatment option could be a drug, researchers say pirfenidone, a drug approved by the FDA for the treatment of idiopathic pulmonary fibrosis. Currently, the drug is also being tested to treat heart failure and chronic kidney disease.
In conclusion, this study is the first to describe the mechanism by which mLOY in the blood causes disease in other organs and to further identify possible treatments. The results showed that mLOY in a certain type of white blood cell in the mouse heart stimulates a known signaling pathway that leads to increased fibrosis. When the researchers blocked this signaling pathway, the cardiac pathological changes caused by mLOY could be reversed.
Paper link: strong>
DOI: 10.1126/science.abn3100< /p>
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