2024-10-17 11:33:00
The study by the University of Oviedo and the CNIC made it possible to identify the EndMT process as a new mechanism involved in this pathological process. Atherosclerosis begins the path to cardiovascular disease.
A team of University of Oviedo and the The National Cardiovascular Research Center (CNIC) has described a new mechanism involved in premature atherosclerosis, which lays the foundations for the identification of a new therapeutic target in the management of premature aging.
The discovery is particularly relevant to the approach to Hutchinson-Gilford syndrome, also known as progeria, a very rare genetic disease that occurs with aging during childhood and adolescence. In fact, premature death usually occurs at an average age of 14.5 years, mainly due to myocardial infarction, heart failure or brain stroke.
The study, conducted by Magda Hamczyk, researcher at the University of Oviedo and visiting scientist at the CNIC, and Vicente Andrés, principal researcher of the Molecular Cardiovascular Physiopathology and Genetics Group of the CNIC and of the CIBER of Cardiovascular Diseases (CIBERCV), achieved It is possible to identify the EndMT (Endothelial-to-MesenchymalTransition) process as a new mechanism involved in this pathological process. The results, published in the journal Circulationwith maximum impact in their area of knowledge, they also propose a new therapeutic target for this disease.
Atherosclerosis consists of the abnormal accumulation of cells and cholesterol in the walls of the arteries. These buildups, called atherosclerotic plaques, lead to hardening and blockage of blood vessels. Furthermore, rupture of the plaques can cause the formation of blood clots and cause a myocardial infarction or stroke, putting the life of the affected person at risk. Given that cardiovascular events are the main cause of death in the world, “research in this field is fundamental to extend the lives of patients suffering from atherosclerosis and prevent complications”, explains Vicente Andrés.
The formation of atherosclerotic plaques progresses silently throughout life and usually manifests clinically after middle age. However, there are some diseases that cause accelerated atherosclerosis and which, in turn, cause premature death. One of the most striking examples is the aforementioned Hutchinson-Gilford syndrome.
Endothelial dysfunction in progeria
Prior to this new work, Vicente Andrés’ group, in collaboration with the team led by Carlos López-Otín, professor of Biochemistry and Molecular Biology at the University of Oviedo, generated a mouse model that suffers from the same symptoms as progeria patientsincluding early atherosclerotic disease. Furthermore, the authors demonstrated that one of the main causes of accelerated atherosclerosis associated with this syndrome is death of vascular smooth muscle cells in the arterial wall.
The new study now published made it possible to study how alterations in vascular smooth muscle cells affect endothelial cells, a type of cell that separates the arterial wall from the blood.
Rosa Nevado, co-author of the study, highlights that “in progeria, the loss of smooth muscle cells induces a series of pathological alterations in endothelial cells.” Additionally, “these changes include the recruitment of immune cells and increased permeability to LDL (called bad cholesterol), processes that can accelerate the formation of atherosclerotic plaques,” adds Hamczyk.
However, the most striking feature of endothelial cells in progeria is the hyperactivation of a phenotypic modulation process called EndMTsays Víctor Quesada, a researcher who also participated in the carrying out of this study. Covadonga Diaz
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Title: Unveiling New Horizons in Atherosclerosis Research: An Interview with Vicente Andrés
Editor (Time.news): Welcome, Vicente. Thank you for joining us today. Your team at the University of Oviedo and the CNIC has unveiled some exciting discoveries regarding atherosclerosis. Can you summarize the key findings and their implications?
Vicente Andrés: Thank you for having me. Our research has identified the Endothelial-to-Mesenchymal Transition, or EndMT, as a significant new mechanism involved in premature atherosclerosis. This is particularly relevant not just for understanding atherosclerosis in general but also for conditions like Hutchinson-Gilford syndrome, which leads to rapid aging in childhood. The insights from our study could pave the way for novel therapeutic strategies to manage premature aging and its cardiovascular implications.
Editor: That’s fascinating! For our readers who might be unfamiliar, could you explain what atherosclerosis is and how it leads to cardiovascular diseases?
Vicente Andrés: Atherosclerosis is characterized by the abnormal buildup of cells, cholesterol, and other substances in the arterial walls, leading to plaque formation. Over time, these plaques can harden and restrict blood flow. Complications arise when plaques rupture, potentially leading to blood clots, myocardial infarctions, or strokes. Given that cardiovascular events are the leading cause of death globally, understanding and preventing this pathology is essential.
Editor: Your findings have significant implications for Hutchinson-Gilford syndrome, a rare genetic disorder. Can you elaborate on the connection between your research and this condition?
Vicente Andrés: Absolutely. Hutchinson-Gilford syndrome accelerates the aging process due to a genetic defect, leading to premature cardiovascular diseases. Our study highlights how the EndMT process contributes to the accelerated atherosclerosis observed in these patients. By targeting this mechanism, we hope to develop therapeutic approaches that could extend the lifespan and improve the quality of life for those affected by this syndrome.
Editor: It sounds like your research could offer hope to many. What was the most challenging aspect of conducting this study?
Vicente Andrés: One of the primary challenges was establishing the connection between EndMT and the pathological processes of atherosclerosis. We had to navigate complex cellular mechanisms and validate our findings across various models. Collaboration with other experts, like Professor Carlos López-Otín’s team, was crucial to overcoming these challenges and ensuring that our research was comprehensive.
Editor: Collaboration seems essential in scientific research. Given the urgency of cardiovascular diseases, how do you see the future of research in this area?
Vicente Andrés: The future looks promising, but there’s still much work to be done. Continued research into the underlying mechanisms of atherosclerosis and related diseases will be vital. We also need to translate our findings into practical therapies. I believe we are on the threshold of significant advancements in therapies targeting cardiovascular diseases, particularly those like progeria that require urgent intervention.
Editor: Before we wrap up, what message would you like to share with our readers about the significance of your work?
Vicente Andrés: I would like to emphasize that foundational research, such as ours on EndMT and atherosclerosis, is vital. It not only enhances our understanding of disease mechanisms but also opens new doors for therapeutics that can potentially save lives. Cardiovascular health is an issue that affects everyone, and public awareness and support for ongoing research can lead to breakthroughs that improve and extend lives.
Editor: Thank you, Vicente. Your insights into this important area of research are invaluable. We look forward to seeing how your work evolves and the impact it will have.
Vicente Andrés: Thank you for the opportunity! It was a pleasure discussing our research with you.