After studying the formation of the heart in utero, a pharmacology researcher from the University of Houston is now reporting on the behavior of cells and molecules during this early development. The researcher is also exploring the potential causes of left ventricular non-compaction (LVNC), a type of heart disease that is also known as spongy heart. Patients with LVNC often require heart transplants. LVNC is a type of heart muscle disease, also known as cardiomyopathy.
Many patients often need heart transplants due to their condition.
According to Mingfu Wu, absence of the Itgb1 gene can lead to problems in the development of the heart, resulting in left ventricular non-compaction. Wu, an associate professor at the UH College of Pharmacy, published these findings in Cardiovascular Research. “Deletion of Itgb1 at an early stage can cause significant defects,” Wu explains.
Wu’s research focused on the examination of trabeculae, which are sheet-like structures that develop in the heart and protrude from the heart wall. These structures play a critical role in early heart development before The coronary system develops to provide an increased inner surface area of the heart wall and improve the exchange of oxygen and nutrients between blood and the heart wall. According to Wu, without trabeculae, the heart wall would not receive enough oxygen and nutrients, potentially leading to death. Conversely, an excessive amount of trabeculae can result in an overly porous heart wall, leading to left ventricular non-compaction cardiomyopathy, also known as spongy heart. While some signals controlling trabeculae formation are known, the exact mechanisms by which individual cells that make up the cardiac muscle (cCardiomyocytes are responsible for forming the structures in the heart wall, but the exact way in which they are organized remains unclear. According to the study, removing a gene called Itgb1 in heart wall cardiomyocytes prevents the formation of trabeculae. It was discovered that the protein β1 integrin encoded by Itgb1 and its ligands, the extracellular matrix, create a molecular network that acts as a scaffold for cardiomyocytes in the heart wall. When Itgb1 is deleted, cardiomyocytes disengage from this scaffold, leading to a loss of their ability to maintain shape, divide properly, migrate, and form trabeculae. The study proposes that this molecular network may be a common mechanism for organizing organs.Information.
“These findings will likely captivate researchers in the field of organ development and regeneration, potentially revolutionizing our comprehension of tissue structure and growth,” stated Wu.
Wu’s colleagues from the University of Houston, including Lianjie Miao, Yangyang Lu, Anika Nusrat, Luqi Zhao Micah Castillo, Yongqi Xiao, Hongyang Guo, Yu Liu, Preethi Gunaratne, Robert, J Schwartz, Alan R Burns, Ashok Kumar, and C. Michael DiPersio, Albany Medical College.
