New Link Between Powerhouse Protein and Heart Failure Made

New Link Between Powerhouse Protein and Heart Failure Made

Posted by Leanne Kodsman on

Starting in high school biology, were taught that mitochondria are the powerhouses of the cell. Further down the line, we learn that mutations or malfunctions within the powerhouse can cause a host of problems including disease states. Researchers at Case Western Reserve University discovered a protein called Kruppel-like Factor 4 (KLF4) that is essential to boosting energy production within mitochondria. More importantly they noted that an absence of KLF4 reduced the production of energy, producing a phenotype that is extremely problematic for cardiac cells.


Starting in high school biology, were taught that mitochondria are the powerhouses of the cell. Further down the line, we learn that mutations or malfunctions within the powerhouse can cause a host of problems including disease states. Researchers at Case Western Reserve University discovered a protein called Kruppel-like Factor 4 (KLF4) that is essential to boosting energy production within mitochondria. More importantly they noted that an absence of KLF4 reduced the production of energy, producing a phenotype that is extremely problematic for cardiac cells. "Some cells are incredibly dependent on mitochondria, particularly the heart and brain," explained lead author Xudong Liao, Ph.D., an assistant professor of medicine at Case Western Reserve University School of Medicine, in the GEN article. "The brain is working all the time, too, even while we are sleeping, so it is particularly sensitive to mitochondrial function. Cancer also hijacks mitochondrial machinery to drive its spread. Therefore, the identification of KLF4 as a major regulator of mitochondrial health may have implications beyond those we detailed in this article." KLFs regulate gene expression in many tissues. According to the article, KLF4 is involved in mitochondrial biogenesis, metabolic function, dynamics and autophagic clearance. Looking at adult mice, researchers found that a deficiency of cardiac specific KLF4 had a potent effect on heart failure. They compared cardiac stress on normal mice and mice who had had the KLF4 gene knocked out. Nearly 50% of the knock out mice were overtaken by heart failure in a week and the rest had a stark decline in cardiac production. Researchers hope that this study will provide the building blocks for further examination of KLF4 in tissues and possibly understand heart disease better.

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