World Heart Day, September 29 Focus on heart health! These research results are worth reading!

Jessica Pfleger says FoxO1 is a major transcription factor that regulates the expression of genes involved in metabolism and growth, but in the heart, foxO1 activity may be closely linked to an increase or decrease in heart growth, and we are not sure what effect FoxO1 activation will have on heart hypertro fertility.
It is important to clarify the key role FoxO1 plays in the heart so that pharmaceutical companies can target new treatments for heart hypertrophy, and in order for these therapies to work more effectively, researchers need to clarify the activation of FoxO1 and its downstream effects.
Cell: Uncovering the molecular mechanism by which the body regulates the growth of scar tissue in the heart after a heart attack! Doi:10.1016/j.cell.2020.06.030 In a recent study published in the international journal Cell, scientists from the University of California and other institutions explained why some people leave wider scars than others after a heart attack. A special protein called type 5 collagen plays a key role in regulating the size of the heart scar tissue, which, once formed, will remain in place for life, reducing the heart's ability to pump blood, thereby increasing the pressure on the remaining heart muscle, and the greater the risk of heart rate problems, heart failure and sudden cardiac death in patients with larger scar tissue sizes.
researcher Dr Arjun Deb said that two people with the same level of heart attack would eventually have different amounts of scar tissue, and given the association between scar size and survival, we wanted to study why some people have more scar tissue in their hearts than others, and if they could reduce it, researchers might be able to improve survival.
After a heart attack, connective tissue cells called fibroblasts secrete a variety of proteins that, when combined, form scar tissue, the vast majority of which are collagen, including type 26, all of which function like glue.
photo Source: JCI Insight: Slow release of two drugs to protect the heart from heart disease! doi:10.1172/jci.insight.132796 In two animal models, a new treatment reduced heart damage after a severe heart attack.
injection of two chemicals in the form of slow release significantly reduced the size of dead heart tissue, known as infarction, and improved the function of the left cardiac chamber compared to the un treated subjects.
risk of death after an acute heart attack is directly related to the size of the infarction, so reducing the size of the infarction is valuable.
heart attack patients form scar tissue to replace dead and dead heart muscle tissue, and over time, as the damaged heart struggles to maintain pumping capacity, it usually develops aggressive heart failure.
study of the new treatment by the University of Alabama at Birmingham (UAB) was published in JCI Insight.
these two chemicals are FGF1 and CHIR99021 (CHIR).
FGF1 is a fibroblast growth factor, CHIR is the activator of the Wnt signaling path, a set of signaling transductors that begin with a protein that transmits signals to the cell through a cell surface subject.
both drugs have shown some benefits, but have never been tested in concert.
7 in-depth interpretation! Scientists have successfully mapped the first 3-D map of neurons in the human heart! doi:10.1016/j.isci.2020.101140, according to a study published in the international journal iScience entitled "A Comprehensive Integrated Anatomical and Molecular Atlas Of Rat Intrinsic Cardiac Nervous System", from Thomas Jeffery Scientists at the University ofSon and others have developed the first 3-D map of human heart neurons; the normal function of the body's heart is maintained by the body's control center, the brain, through a very complex neural network that can trigger heart attacks, including heart attacks, sudden cardiac death and blood supply problems, when this "communication" is disrupted.
as an additional layer of safety, the heart has its own "small brain", called the nervous system in the heart (ICN, intracardiac nervous system), which monitors and corrects any barriers to communication.
ICN is important for supporting heart health, even protecting the heart muscle from damage in the event of a heart attack, but researchers don't yet know how ICN works because they don't know how the neurons that make up the ICP are organized, where they are located in the heart, how they connect to each other, and what their molecular properties are.
study, the researchers answered these questions in unprecedented detail.
a major breakthrough in the Nature sub-journal! Activating cancer genes can regenerate the heart! Doi:10.1038/s41467-020-15552-x Researchers tried to turn off a gene that allows cancer to spread, only to make a surprise 180-degree turn.
by making the gene overactive and functional in the heart of mice, they trigger the regeneration of heart cells.
the power of this gene represents a significant advance in the first cure for heart disease, as adults' hearts are often unable to repair themselves if they are damaged.
Catherine Wilson, a pharmacologist at the University of Cambridge who led the study, said: "It's really exciting because scientists have been trying to multiply heart cells.
current treatments for heart disease do not reverse the degeneration of heart tissue - they can only slow the progression of the disease.
now, we've found a way to do this on the mouse model.
" in mammalian cells, the cell cycle of cell self-replication is strictly controlled.
cancer occurs when cells begin to replicate uncontrolled, and the Myc gene plays a key role in this process.
myc is known to be too active in most cancers, so research into the gene is one of the top priorities in cancer research.
recent studies have focused on trying to control Myc as a cancer treatment.
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