In a new study from the University of Virginia School of Medicine, scientists led by Dr. Mete Civelek have made significant strides in understanding cardiovascular diseases. Specifically, they have delved into atherosclerosis, which is the hardening of arteries due to fatty plaque buildup.
Atherosclerosis causes fibrous caps to form over plaques, serving as a protective barrier against dislodging, triggering heart attacks, or strokes. Dr. Civelek’s team concentrated on the biological “scaffolding” created over plaques, viewing it as key in fighting the top cause of global death.
The innovative approach merged two decades of human genetics findings with a unique collection of smooth muscle cells from arteries. This combination targeted the development site for these plaques.
“We discovered that our genetic makeup impacts the ways smooth muscle cells secrete proteins that provide strength to plaques and prevent them from rupturing,” Dr. Civelek explained, highlighting the potential for these insights to lead to lifesaving treatments.
The research meticulously centers on the “extracellular matrix,” a protein-rich, glue-like substance, which is secreted by smooth muscle cells. Consequently, it forms the protective scaffolding over plaques, ensuring structural integrity and support.
By meticulously analyzing these proteins in cells from 123 heart transplant donors, the team diligently traced back. The goal was to identify genes responsible for their prolific production, emphasizing genetic contributions.
This thorough process uncovered 20 genetic locations directly related to the critical proteins, revealing intricate relationships. Moreover, it pinpointed a gene variation, significantly linked to an increased risk. This variation notably influences the hardening of arteries, highlighting potential targets for therapeutic intervention.
These discoveries are pivotal for identifying individuals at high risk of plaque rupture, offering new avenues for preventative care.
Furthermore, the study revealed the dual nature of smooth muscle cell efforts in plaque formation – sometimes protective, other times harmful. This nuanced understanding opens the door to targeted treatments for atherosclerosis and related cardiovascular conditions.
One particular protein, LTBP1, emerged as a key player in plaque stability. “We identified LTBP1 as a significant factor in the stability of these plaques,” Civelek stated, underscoring the team’s commitment to further research this protein as a therapeutic target.
The University of Virginia’s research marks a crucial step forward in cardiovascular disease treatment, significantly advancing our understanding.
Importantly, by linking genetic factors to the body’s defenses against artery plaque, this study offers a personalized medicine roadmap, enhancing cardiovascular risk comprehension. The research also paves the way for innovative treatments, potentially reducing heart disease’s global burden significantly.
As Dr. Civelek and his team continue their research, focusing on translating findings into patient care remains paramount. With a better grasp of atherosclerosis and cardiovascular diseases’ genetic bases, the medical community is now equipped to develop tailored treatments, offering hope globally.
Cardiovascular disease (CVD) refers to disorders that affect the heart and blood vessels, and it stands as a leading cause of morbidity and mortality across the globe. The spectrum of CVD includes various conditions, each with its own set of causes, symptoms, and treatment options.
One prevalent form of CVD is coronary artery disease (CAD), characterized by the buildup of plaque in the coronary arteries that supply blood to the heart. This buildup can lead to chest pain, heart attacks, and other serious complications.
Another significant category within CVD is stroke, which arises when blood flow to a part of the brain is interrupted, leading to brain damage and various long-term disabilities.
Other forms of cardiovascular disease include heart failure, a condition where the heart is unable to pump blood effectively throughout the body; arrhythmias, which are irregular heartbeats that can affect how well the heart works; and heart valve problems, where the valves that control blood flow in and out of the heart’s chambers don’t function properly.
Risk factors for developing CVD include high blood pressure, high cholesterol, smoking, diabetes, obesity, physical inactivity, and an unhealthy diet, among others.
Prevention and treatment strategies focus on managing these risk factors through lifestyle changes, medications, and in some cases, surgical interventions.
Regular check-ups and monitoring are crucial for early detection and management of the disease, ultimately improving outcomes and quality of life for those affected.
The study is published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology.
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