A team of researchers from Kumamoto University, headed by Prof. Yuichi Oike, has found a new mechanism of heart failure and developed a gene therapy to combat this fatal disorder. Heart failure is a condition in which the heart does not pump adequate blood as it should. It is a leading cause of death that affects approximately 23 million people in the world. Despite many years of intensive research, heart failure cannot be cured. Current drugs can only improve symptoms to some extent. Oike's team discovered that a protein, called Angiopoietin-like protein 2 (ANGPTL2), accelerates the progression of heart failure. ANGPTL2 is secreted by cardiac muscle cells and can disturb heart function. Mice overexpressing this protein in the heart exhibited heart dysfunction, while mice that did not produce Angptl2 had increased left ventricular contractility and up-regulated energy metabolism. The findings were published online Sep. 28 in the journal Nature Communications. In previous studies, Oike's team revealed that, when aged or stressed cells secrete too much ANGPTL2, the protein can trigger chronic inflammation and increase the risk of atherosclerosis and other diseases. In this work, they discovered that cardiac muscle cells from patients with heart failure produced and secreted more ANGPTL2. Using mice that lacked ANGPLT2, the researchers found that the progression of heart failure was inhibited. In further experiments, the team developed a novel gene therapy that can inhibit ANGPLT2 production in cardiac muscle cells. Then they tested the gene therapy in a mouse model of heart failure, and found that ANGPTL2 production in cardiac muscle cells was decreased and the progression of heart failure was suppressed. When the team conducted related experiments in cardiac muscle cells that were differentiated from human iPS cells, they found similar results. The data demonstrated the therapeutic effect of the gene therapy. CusAb offers Recombinant TMPRSS15, you will get to know our products on our website.
