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    Home > Medical News > Medical Research Articles > Heart failure occurs after a heart attack, and an enzyme is key

    Heart failure occurs after a heart attack, and an enzyme is key

    • Last Update: 2021-03-08
    • Source: Internet
    • Author: User
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    heart failure after myocardial infarction? Researchers at the Army Medical University's Army Specialty Medical Center have found and confirmed that the high expression of G protein-coupled complex kinase 4 (GRK4) after heart attack may be the culprit of heart failure, inhibiting GRK4 to protect heart function after heart attack and reduce myocardial apoptosis. The findings were published online December 7 in the Journal of the European Heart.The loss of a large number of myocardial cells due to apoptosis after myocardial infarction is the pathological basis for heart failure and clinical death. More than 70 percent of patients treated after a heart attack develop heart failure within five years. This is because myocardial cells are hit and some cells slowly die, leading to heart failure. In recent years, heart failure therapy has gradually formed a β "golden triangle" for atTA1, technology and other subjects.“ Through experiments, we found that GRK4 in the heart muscle after myocardial infarction from nothing, the expression increased significantly, so we further studied the effect of GRK4 on myocardial infarction and its mechanism. Zeng Chunyu, director of cardiovascular medicine at the Army Specialty Medical Center at the Army Medical University, said.The researchers constructed GRK4 wild type and GRK4 A486V genetically modified mice, as well as myocardial-specific GRK4 knock-out mice, through the heart attack experiment, from both positive and opposite aspects showed that the expression of GRK4 worsens heart function, increases the area of myocardial infarction, promotes myocardial apoptosis, inhibits GRK4 plays a protective role. In addition, the researchers studied A486V, the most common variant of GRK4 in Asians. They found that patients with the A486V variant had significantly worse postcardial function than the control group. This shows that patients with A486V variants are clinically worthy of attention.At present, the research team has carried out the study of GRK4 inhibitors. Zeng Chunyu said that inhibiting GRK4 as a prevention target for heart failure after heart attack may further reduce the incidence of heart failure after heart attack in the case of heart failure "Golden Triangle" treatment.
    (Science and Technology Daily)
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