Debate on the health benefits of "rejuvenated" protein

According to a new study led by scientists at the University of California, San Francisco (UCSF), people who were previously diagnosed with heart disease were less likely to experience heart failure, heart attack or moderate wind, or die from these events, if their blood levels were high for two very closely related proteins One of these proteins, known as Gdf11, has been of great interest since 2013, when researchers found it could make aging mice younger Based on these findings, scientists speculate that drugs that increase Gdf11 levels may reverse the physiological performance of aging, which can lead to heart failure, in humans However, a study published in cell metabolism in May this year questioned this mainstream theory Extended reading: the anti-aging research of cell and science is questioned: who has promoted the rejuvenation of children? The new study was published in European heart on August 20 Journal (impact factor 15.203), the team used new technology to identify and measure a group of proteins in the blood, which may be related to poor health results, which can be used as a measure to estimate the risk of a person having various cardiovascular problems, as well as their risk of death from cardiovascular disease The study population consisted of 1899 men and women with heart disease, from different research groups in San Francisco and Norway, aged 40 to 85 (average 69) They have been diagnosed with stable ischemic heart disease, which results in reduced blood supply to the heart and an increased risk of stroke, heart attack, hospitalization for heart failure and death in subjects due to coronary artery disease During the course of the study, hundreds of participants were monitored for nearly nine years, and they presented one or more of these outcomes The research team of UCSF, led by Professor Peter Ganz, director of Cardiology, San Francisco General Hospital and trauma center of UCSF cooperation hospital, used a laboratory test to measure the blood level of Gdf11 and a very similar protein (called myogenic inhibitory protein), which could not distinguish the two, because they are very similar in structure and function At the beginning of the study, the scientists found that some subjects had relatively high levels of these proteins in their blood (the first 25% of all subjects), and that they were less than half likely to die of any cause compared to the last 25% of subjects The top 25% of subjects also experienced fewer adverse health events related to heart disease "People with heart disease, if they have relatively high concentrations of these proteins, are much less likely to die and experience the devastating consequences of aging, including heart disease, stroke and heart failure," Ganz said We also found that the level of Gdf11 and myogenin decreased with age in humans, but the degree of this decline was different among individuals " In the mouse research published in cell in 2013 and Science in 2014, a research team led by Dr Richard Lee and Amy wagers of Harvard Medical School reported that compared with young mice, older mice have less Gdf11 in their blood circulation They also found that after four weeks of Gdf11 treatment, the protein returned to a younger level, possibly reversing potentially harmful cardiac muscle thickening In the human body, this thickening of the heart muscle, known as ventricular hypertrophy, is related to aging and can cause heart failure and death In this new study, UCSF researchers measured ventricular hypertrophy using standard clinical imaging tests and found that subjects with lower levels of Gdf11 and myostatin were more likely to develop cardiac hypertrophy "This association with ventricular hypertrophy and reduced mortality suggests that Gdf11 may play the same role in humans as in mice," Ganz said Restoring Gdf11 or myostatin to a higher, younger level is likely to be a so-called "fountain of youth" treatment, but more needs to be done " Subjects with higher levels of Gdf11 and myostatin had fewer heart disease-related deaths, which did not fully explain the magnitude of fewer deaths from various causes in this group It is possible that Gdf11 and myostatin can also prevent death unrelated to heart disease In addition to finding ways to raise the level of Gdf11 or myostatin, Ganz and his colleagues suggest another way to improve health outcomes: blocking the action of a circulating protein, called FSTL3, which inhibits the action of myostatin and Gdf11 At the March meeting of the American Heart Association, Ganz's laboratory team reported preliminary evidence that high FSTL3 levels are associated with poor health in heart attack patients "If the potential health benefits of higher levels of Gdf11 and myostatin seem to outweigh the risks, at least in patients with heart disease, it might be easier to get rid of inhibitors of Gdf11 and myostatin rather than replace lower levels of proteins," Ganz said