The article "Myocardial reprogramming by HMGN1 underlies heart defects in trisomy 21" is published in the journal Nature and can be found at the following DOI: https://doi.org/10.1038/s41586-025-09593-9.
The article discusses how a specific protein called HMGN1 is involved in causing heart defects in individuals with trisomy 21, a genetic disorder that affects about 1 in 250 people worldwide. The study found that HMGN1 causes the reprogramming of myocardial cells (heart muscle cells) to become defective and lead to heart problems.
Trisomy 21 is caused by an extra copy of chromosome 21, which leads to a range of health problems, including intellectual disability, developmental delays, and increased risk of premature death. The article suggests that HMGN1 may play a key role in the development of these heart defects, which are often fatal.
The study used a combination of genetic analysis and animal models to investigate the role of HMGN1 in heart disease. The researchers found that HMGN1 is highly expressed in the hearts of individuals with trisomy 21, and that it causes changes in the gene expression profile of cardiac cells, leading to the development of defective myocardial tissue.
The study's findings have important implications for our understanding of the genetic basis of heart disease and may lead to new therapeutic strategies for treating trisomy 21-related heart defects.
The article discusses how a specific protein called HMGN1 is involved in causing heart defects in individuals with trisomy 21, a genetic disorder that affects about 1 in 250 people worldwide. The study found that HMGN1 causes the reprogramming of myocardial cells (heart muscle cells) to become defective and lead to heart problems.
Trisomy 21 is caused by an extra copy of chromosome 21, which leads to a range of health problems, including intellectual disability, developmental delays, and increased risk of premature death. The article suggests that HMGN1 may play a key role in the development of these heart defects, which are often fatal.
The study used a combination of genetic analysis and animal models to investigate the role of HMGN1 in heart disease. The researchers found that HMGN1 is highly expressed in the hearts of individuals with trisomy 21, and that it causes changes in the gene expression profile of cardiac cells, leading to the development of defective myocardial tissue.
The study's findings have important implications for our understanding of the genetic basis of heart disease and may lead to new therapeutic strategies for treating trisomy 21-related heart defects.