Discovery of a previously unknown heart muscle protein and how it affects mechanisms related to heart failure may lead to further treatments for cardiovascular disease.
Discovery of a previously unknown heart muscle protein and how it affects mechanisms related to heart failure may lead to further treatments for cardiovascular disease, according to a study published in Nature Communications.
Cardiologists Dr Matthias Eden and Professor Norbert Frey, from the University of Kiel in Germany, have recently discovered the Myoscape/FAM40B/STRIP2 protein, and how it directly affects the L-type calcium channel (LTCC). Specifically, the Myoscape protein influences calcium metabolism and the pumping ability of the heart muscle cell.
“In the absence of Myoscape, heart muscle cells in the model system develop a serious impairment of calcium channel metabolism, ultimately leading to progressive heart failure,” Frey said in a statement.
Combined with the protein actinin 2, Myoscape stabilizes the LTCC in the heart muscle cell at the necessary position within the cell membrane. Using Myoscape-depleted morphant zebrafish and Myoscape knockout mice, the researchers noted that without the Myoscape protein the calcium channel metabolism of the heart muscle cells became impaired and progressed to advanced heart failure. The mice, for example, depicted a reduction in LTCC currents, cell capacity, and calcium current densities.
When artificially increasing the levels of Myoscape, the researchers saw that the calcium channel currents increased as well. As such, Myoscape seems to restore previously decreased calcium currents in failing heart muscle cells.
“Since patients with severe heart failure also exhibit reduced levels of Myoscape protein in the heart, we believe that we have here discovered a critical new mechanism for the genesis of heart failure,” Frey said. With this dual discovery, it is possible that innovative new treatments will follow.