Articles tagged with Vascular Smooth Muscle Cells
Research reveals DKK3's role in AAA progression through phenotypic switching of vascular smooth muscle cells, driven by the TGFβ3-Smad2/3 axis. This study identifies DKK3 as a potential therapeutic target for maintaining VSMC homeostasis in AAA.
Researchers at the University of Virginia Health System have identified a crucial biological switch that regulates renin production in certain cells, allowing them to control blood pressure. This discovery provides important direction for future research into high blood pressure and cardiovascular disease treatment.
Researchers at CNIC have identified endothelial-to-mesenchymal transition as a novel mechanism in premature atherosclerosis in progeria. The study proposes a new therapeutic target for this disease and highlights the importance of investigating rare diseases like progeria.
Researchers developed DNA aptamer iSN04 to target vascular smooth muscle cells, reducing plaque formation and promoting stability. The study showed that iSN04 can effectively enter VSMCs without carriers, inducing differentiation and inhibiting angiogenesis.
Scientists have developed a functional model of thoracic aortic aneurysm using human cells in laboratory rats, offering new avenues for drug development and effective screening. The model successfully mimics dilation of the human aorta and has potential applications for treating this potentially fatal condition.
Researchers discovered that eliminating progerin from vascular smooth muscle cells prevents atherosclerosis and improves life expectancy in HGPSrev mice. This finding suggests a potential therapeutic strategy for treating progeria, an extremely rare genetic disease affecting 1 in every 20 million people.
Researchers at UVA Health System have discovered genetic clues that may help identify people at risk of cardiovascular disease, including atherosclerosis. The study identified 20 locations on chromosomes that influence protein production, shedding light on why smooth muscle cells sometimes are beneficial and sometimes harmful.
Yabing Chen has received two NIH grants totaling over $5 million to investigate vascular diseases and their link to dementia. Her research focuses on Runx2, a master transcription factor involved in both bone formation and calcification of arteries.
Researchers discovered that a mutation in the gene ACTA2 causes moyamoya disease and strokes in young children. The mutation leads to dysfunctional smooth muscle cells in arteries, resulting in blockages and increased risk of stroke. Understanding this mechanism could lead to new treatments for moyamoya disease.
A new study has created the world's largest map of normal breast tissue, highlighting 12 major cell types and 58 biological cell states. The atlas also identifies differences based on ethnicity, age, and menopause status, providing a powerful resource for researchers studying breast cancer and other diseases.
CARMN is a long noncoding RNA that regulates contractility in both blood vessels and the gastrointestinal tract. Without CARMN, mice cannot survive due to impaired GI tract contraction, leading to conditions like intestinal pseudo-obstruction.
Researchers found that when FXR1 is absent, vascular smooth muscle cells proliferate more slowly, become senescent, and scar tissue development is reduced. This suggests that drugs targeting FXR1 may treat vascular proliferative diseases such as atherosclerosis, restenosis, hypertension, and abdominal aortic aneurysm.
Research by Whitehead et al. reveals that cellular senescence triggers amyloidosis through changes in small extracellular vesicles and extracellular matrix composition. The study provides novel insights into the formation of aortic medial amyloid and offers potential therapeutic targets for mitigating its effects.
Researchers discover that inhibiting a gene crucial for DNA production can significantly reduce destructive cell proliferation and disease progression in pulmonary hypertension. This finding presents a potential treatment target for the condition, which affects females aged 30-60 with limited treatment options.
Vascular diseases such as atherosclerosis are associated with the reorganization of blood vessel structure through transdifferentiation. The researchers discovered that endothelial cells can transdifferentiate into smooth muscle cells, driven by HIF1α, and that this process contributes to neointima formation.
Scientists at Medical College of Georgia discover a new target to intervene in coronary artery disease, the most common type of heart disease. The target is ATIC, a gene essential for purine production, which increases in response to arterial disease.
Researchers aim to understand the role of FAK in promoting key changes in vascular smooth muscle cells that contribute to atherosclerosis. Preliminary evidence suggests that inhibiting FAK may block VSMC transdifferentiation and promote plaque stability.
Scientists aim to improve vein health for patients undergoing heart bypass surgery and dialysis. They discovered that two genes play a crucial role in smooth muscle cell differentiation, enabling veins to mature and function like arteries.
Scientists found that a single 45-minute session of moderate-intensity exercise enables the growth of new blood vessels in people with type 2 diabetes. The exercise increases levels of ATP7A, a protein carried by exosomes that helps deliver essential copper to endothelial cells, promoting angiogenesis and reducing oxidative stress.
Researchers at NYU Tandon have discovered the mechanical basis for abdominal aortic aneurysm (AAA), a complex vascular disease. They identified Piezo1, a novel culprit of mechanically fatigued aorta in AAA, and found that inhibition of Piezo1 prevents mice from developing AAA by alleviating pathological vascular remodeling.
A molecule of RNA called CARMN has been found to play a crucial role in maintaining healthy smooth muscle cells in the blood vessel wall, which can help prevent atherosclerosis and angioplasty-induced restenosis. Restoring healthy CARMN levels may lead to new approaches for treating heart disease.
Research from the University of Virginia Health System found that long-term use of ACE inhibitors and angiotensin receptor blockers can lead to hardened kidney vessels. The drugs, commonly prescribed for high blood pressure and heart failure, were associated with damage in both lab mice and humans.
Recent clinical and experimental data suggest that vascular calcification and bone loss share common pathophysiological mechanisms. The International Osteoporosis Foundation's new review elucidates the key associations between the two disorders.
Researchers at Nanyang Technological University have developed a 3D model of the human artery blood vessel wall to study atherosclerosis. The model, called an 'arterial wall-on-a-chip', helps understand how cholesterol and inflammatory cells contribute to the disease.
Researchers from the University of Tsukuba found that PDGFRa+ cells in the adventitia contribute to neointima formation, a process where blood vessels thicken and cause blockages. The type of injury inflicted on blood vessels affects how these cells respond.
A new vasculogenic niche contributes to cardiac lymphatic system development, with cells originating from different tissues. The coronary lymphatic vessels have varied origins and functions.
Researchers found that activating the apelin receptor led to increased blood pressure due to vasoconstriction, a process also affected by the α1A-adrenergic receptor. The study suggests a coordinated mechanism controlling blood vessel contraction and may support therapy development for vascular stenosis and vasospasm.
Researchers have developed artificial molecules that selectively target abnormal vascular smooth muscle cells without affecting endothelial cells. This could lead to new, safer stent treatments.
Researchers at UVA Health System found that perivascular cells are essential for complete blood vessel formation. The discovery offers new direction for treating conditions like diabetes and heart attacks by growing functional blood vessels.
Researchers have generated the first mouse model of atherosclerosis accelerated by progerin, a protein causing Hutchinson-Gilford syndrome. The study identifies vascular smooth muscle cells as a key target for treating premature atherosclerosis in progeria.
Researchers found that low dietary potassium promotes elevated aortic stiffness, while increased dietary potassium alleviates it. Increased potassium also reduced vascular calcification and aortic stiffness in mouse models, suggesting its potential to protect against heart disease.
Ca2+ plays a crucial role in arteriolar function by triggering vasodilation through endothelial cells. The magnitude of these signals depends on IP3 receptors.
A new study by UNC School of Medicine researchers found that the IRS-1 protein plays a crucial role in maintaining vascular smooth muscle cell differentiation, which helps prevent atherosclerosis. In people with diabetes, low IRS-1 levels contribute to abnormal cellular proliferation and increased risk of heart disease.
Researchers at Joslin Diabetes Center have identified a key role for the SHP-1 enzyme in stent failure in people with diabetes. By suppressing smooth muscle cell growth, SHP-1 may lead to more effective surgical stents.
Researchers find Gli1 positive stem cells, which can become smooth muscle cells, bone-building osteoblasts, and other connective tissues, contribute to vascular calcification. The study provides insights into the active process behind calcified blood vessels in chronic kidney disease.
Research found that angiotensin II-induced hypertension increases with age due to heterodimerization of AT1R with P2Y6R. This altered signaling pathway converts cell proliferation to hypertrophy in vascular smooth muscle cells.
New research reveals that smooth muscle cells surrounding brain blood vessels regulate blood flow in response to neuronal activity. The study contradicts previous theories on pericytes' role in blood vessel formation and function.
Researchers identified smooth muscle cells as a major contributing factor to vascular stiffness, a significant contributor to hypertension. The study's findings suggest that targeting these cells may lead to new possibilities for drug treatments for the disease.
A study by Changcheng Zhou and colleagues found that IKKβ deficiency in smooth muscle cells decreases vascular inflammation and atherosclerosis, while also blocking fat cell differentiation. This suggests a novel therapeutic target for treating obesity, atherosclerosis, and metabolic disorders.
Researchers found that deleting YAP from vascular smooth muscle cells causes thin-walled blood vessels prone to over-dilation and aneurysms. The protein also manages cell proliferation and suppression of the cell cycle arrest gene Gpr132, suggesting its role in normal blood vessel formation.
Research suggests nicotine drives cell invasion contributing to atherosclerosis and plaque formation in coronary arteries. E-cigarettes may not significantly reduce smokers' risk for heart disease, according to Brown University study findings.
Researchers identify markers that can predict rupture in abdominal aortic aneurysms, including dense white blood cells and C-reactive protein levels. The study suggests that PET/CT scans with positive uptake could provide diagnostic support for surgery, while negative uptake may indicate safe avoidance of unnecessary procedures.
Case Western Reserve researchers identified Kruppel-like factor (KLF) 15 as a master regulator of vascular health, blocking blood vessel inflammation that can lead to heart attacks and strokes. The discovery offers hope for targeted anti-inflammatory therapies for vascular disease.
Researchers discovered that compounds derived from polyunsaturated fatty acids (omega-3s) reduce inflammation in acutely injured blood vessels, promoting better artery healing after procedures like angioplasty and bypass surgery. These naturally occurring compounds could improve long-term results of cardiovascular procedures.
Researchers at the Max Planck Institute have discovered how external signals regulate vascular remodelling through G protein-mediated signalling pathways. These pathways work together in other contexts but act as antagonists in blood vessel remodelling, balancing cell growth and regression.
Researchers at the University of California, Berkeley, used genetic tracing to identify a previously unknown type of stem cell as the real culprit behind vascular diseases. This multipotent vascular stem cell is capable of differentiating into various specialized cell types and plays a key role in the calcification of blood vessels.
Scientists at Salk Institute successfully generated induced pluripotent stem cells from patients with Hutchinson-Gilford Progeria Syndrome, a rare disorder that accelerates aging. The cells displayed signs of vascular aging and were differentiated into smooth muscle cells that showed premature aging phenotypes.
Pitt researchers have successfully grown arteries with high elasticity using baboon smooth muscle cells, containing 20% of the protein elastin found in natural arteries. The process resembles how it would be used in a patient and has the potential to overcome a major barrier to creating living-tissue replacements for damaged arteries.
Researchers found that Smurf1 is elevated in animal models of PAH and can degrade BMP receptors, leading to excessive growth of vascular cells. This suggests Smurf1 may be an attractive therapeutic target to block disease progression.
A study led by Akiko Hata of Tufts University School of Medicine found that the heart protein FHL2 regulates blood vessel maintenance. FHL2 inhibits the genes necessary for vascular smooth muscle cells to transition between a resting and proliferative state.
Researchers at Ohio State University identified a genetic link between the profilin 1 gene and increased risk of high blood pressure in older adults. The gene affects vascular remodeling, which can lead to structural and functional changes in blood vessels, ultimately causing hypertension.
Researchers discover GRK5 plays a key role in preventing cell growth and proliferation in blood vessel damage, hinting at alternative therapeutic targets. The study suggests that other cell types, such as epithelial cells or bone marrow derived stem cells, may also contribute to restenosis.
Researchers discover that CA4P selectively targets endothelial cells, inducing regression of unstable blood vessels by disrupting VE-cadherin signaling. This breakthrough could lead to new avenues for targeting tumor neo-vessels and increasing the therapeutic window of anti-angiogenic agents.
Researchers understand the mechanism of smooth muscle cell growth, which allows for contraction and expansion of blood vessels. The discovery opens up new avenues for treating vascular disorders by targeting the Foxo4 protein.
The Duke team successfully engineered new blood vessels from vascular cells of four elderly men with heart disease, extending their lifespan indefinitely. The treated smooth muscle cells were then impregnated into a biodegradable polymer tube and grew for up to seven weeks, forming functional-like arteries.
Researchers discover that MT1-MMP controls blood vessel response to PDGF-ß signaling, essential for normal vessel formation. MT1-MMP-null mice exhibit severely compromised vascular architecture, suggesting potential therapeutic targets for controlling tumor growth and metastasis.
Researchers found a link between high phosphorous levels and vascular calcification, leading to increased risk of cardiac problems. Treatment with an experimental medication alleviated skeletal weakening and decreased signs of vascular calcification in mice.
A study from the Ludwig Institute for Cancer Research has uncovered a fundamental mechanism of lymphatic vessel formation, revealing abnormally shaped vessels covered in smooth muscle cells. The findings may lead to better treatments for lymphedema, which affects people worldwide and can be inherited or caused by tumor removal.
Researchers successfully converted circulating smooth muscle progenitor cells into functional smooth muscle cells, which could help address interventional cardiology problems. The study may pave the way for therapeutic angiogenesis by preventing or eliminating the adhesive properties that contribute to plaque formation.