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A New Molecular Player for Heart Extension for Heart Disease – ScienceDaily

In response to conditions such as high blood pressure and reduced blood flow to the heart muscle, the adult heart can significantly increase the process called pathological hypertrophy, which keeps the heart functioning in the short term, but prefers patients with disability of heart failure and sudden cardiac death if left behind. unprocessed. Now, researchers at the North Carolina Medical School found that the development of pathological hypertrophy requires the binding of RNA binding protein Lin28a.

Published in magazine CirculationThe discovery could have a significant impact on the treatment of stronger heart disease, which is the leading cause of death in the United States and around the world.

"One of the initial stages of gene regulation is transcription of DNA sequences in RNA. However, after regulating transcription with RNA binding proteins, it has become a critical regulatory layer for controlling the function of genes in health and diseases," said Jiandong Liu, PhD, Professor of Pathology and Laboratory Medicine at UNC and Research. senior author. During pathological hypertrophy, the heart undergoes extensive structural changes that are known to be associated with significant changes in cardiac gene expression.

"Identifying Lin28a as a new regulator of abnormal heart hypertrophy adds RNA to transcriptional regulation as a new mechanism that underpins this important heart disease member," Liu added.

One of the major signs of cardiac hypertrophy is metabolic changes because hypertrophic heart is more dependent on glucose metabolism – when glucose is converted into energy cells – than oxidation of fatty acids, which is a different cell of complex process used to create energy.

"It is interesting to note that most of the Lin28a regulated genes in the early phase of hypertrophy of the heart are enriched with metabolic and metabolic pathways, and that Lin28a helps to increase glycolysis and reduces the oxidation of fatty acids in hypertrophic hearts," said Liu also at McCllel Heart Institute at UNC-Chapel Hill. member.

With several research methods, including next-generation sequencing, RNA immunoassay, and gene expression analysis, the Liu study group also identified some of the mechanisms by which Lin28a stimulates hypertrophy. His laboratory found that Lin28a was targeting the gene Pck2, which encodes the major mitochondrial protein needed by the heart to improve glycolysis.

"Our research provides strong evidence that Lin28a plays an important role in the cardiac stress response during pathological hypertrophy," said Liu. "Directly attaching to Pck2 mRNA, Lin28a facilitates an important switch in the metabolic processing required to increase the heart's response to stress. These results are consistent with previous studies, which also revealed that the metabolic switch should occur before the heart can dramatically increase.

In general, Liu's findings confirm the idea that in the early stages of cardiac hypertrophy, the transition to metabolic treatment may be useful for heart restructuring and cardiac response.

"Identification of key genes such as Lin28a and Pck2, which facilitate this switch in heart metabolism and ultimately lead to cardiac enlargement, is an important step in creating possible therapeutic options for those suffering from abnormal hypertrophy and heart failure," Liu said. .

The co-authors of the study are Hong Ma, Shuo Yu, Yingao Zhang, Thomas Fakadej, Ziqing Liu, Chaoying Yin, Joan M. Taylor, and Li Qian from the University of North Carolina at Chapel Hill, Xiaojing Liu, Jason W. University, and Weining Shen, University of California, Irvine. .

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