Cardiovascular Disease (CVD) is a collective term for diseases related to the heart and blood vessels. Heart-related diseases include hypertension, valvular heart disease, inflammatory heart disease, congenital heart disease, rheumatic heart disease, cardiomyopathy, heart failure, pulmonary heart disease, and arrhythmias. Vascular-related diseases encompass coronary artery disease (such as angina and heart attacks), peripheral artery disease, cerebrovascular diseases (including stroke), and renal artery stenosis.
As one of the most significant threats to human health worldwide, cardiovascular diseases have a higher incidence and mortality rate than even cancer, making them the leading cause of global deaths. According to statistics, approximately 17.9 million people die from cardiovascular diseases every year, with over 80% of these deaths attributed to heart attacks and strokes. Research conducted by the Centers for Disease Control (CDC) in the United States revealed that one person dies from cardiovascular disease every 33 seconds in the country. Apart from genetic and environmental factors, unhealthy diet, lack of exercise, smoking, and excessive alcohol consumption are major contributors to the development of cardiovascular diseases.
CUSABIO has curated a selection of high-quality ELISA kits specifically designed for research in the field of cardiovascular diseases. These kits aid in studying the mechanisms behind cardiovascular diseases, changes in biomarkers, and new therapeutic strategies, thus advancing your drug development process.
The narrowing or occlusion of blood supply in the vascular bed is a common characteristic of cardiovascular disease and is often caused by atherosclerosis. Therefore, the treatment of CVD aims to restore blood flow in the affected vascular bed. In the early stages of CVD, the focus is on lifestyle changes for the patients. As the condition worsens, medication or surgical interventions might be necessary to increase blood flow to the affected tissues or reduce energy demands. Drug therapy involves using medications to lower heart rate, thereby reducing oxygen demand, or applying drugs that cause vasodilation to increase blood supply.
One major therapeutic approach in therapeutic angiogenesis involves delivering certain growth factors in the form of proteins or genes encoding target proteins. This induction, enhancement, and regulation of host blood vessel formation helps revascularize ischemic tissues. These growth factors include VEGF, bFGF, HGF, PDGF, ANG-1, and IGF-1, among others.
Thrombus is a kind of clot formed in blood, which is usually composed of fibrin, platelets, red blood cells and other components. The main function of thrombus is to form a "patch" inside the injured blood vessel to prevent excessive bleeding. However, when thrombosis is excessive or formed under inappropriate conditions, it may lead to serious cardiovascular diseases, such as myocardial infarction (MI), acute ischemic stroke (AIS) and venous thromboembolism (VTE).
Fibrinogen is a kind of glycoprotein. When coagulation is triggered, thrombin splits fibrinogen into fibrin, which is aggregated into a fiber network to stabilize thrombus.
Platelets are an important target of antithrombotic therapy. Activated platelets provide negatively charged biofilm, which is very important for the assembly of prothrombinase and tensinase complex.
The interaction of CD95 receptor ligand between red blood cells and activated platelets has been proved to lead to the exposure of phosphatidylserine on platelets and red blood cells, which leads to platelet degranulation and thrombosis.
Von willebrand factor (VWF) is a kind of protein, which plays an important role in the process of blood coagulation. It is produced by megakaryocytes and vascular endothelial cells, which can stabilize coagulation factor VIII and mediate platelet adhesion to vascular injury sites, thus promoting thrombosis. The main pathogenic mechanism of von Willebrand factor is the decrease of plasma VWF quantity or abnormal quality caused by gene mutation.
Blood pressure (BP) is the pressure of circulating blood on the blood vessel wall. Blood pressure regulation is a physiological process in which the body maintains the blood pressure in the circulatory system at an appropriate level. Normal blood pressure regulation is very important for cardiovascular health. Too high or too low blood pressure may cause cardiovascular diseases and other health problems. The mechanism of blood pressure regulation is complex and diverse, among which Renin-Angiotensin-Aldosterone System (RAAS) is the most clear, which can regulate and maintain the balance of blood pressure, water and electrolyte and systemic vascular resistance.
Hypoxia refers to the deprivation of oxygen reaching body tissues (such as brain and heart), which can be almost fatal. There are different types of hypoxia, including hypotonic hypoxia, blood hypoxia, circulatory hypoxia and tissue toxic hypoxia. The activation of hypoxia-induced signal transduction mechanism is an important condition for the development of most cardiovascular diseases, which involves transcription factors (HIF-1, NF-kβ), the coordination between reactive oxygen species and downstream effector molecules.
Cholesterol is a necessary sterol molecule for maintaining cell membrane, regulating membrane fluidity and establishing membrane permeability. High density lipoprotein cholesterol (HDL-C) helps to reduce the risk of cardiovascular diseases, while low density lipoprotein cholesterol (LDL-C) is regarded as a risk factor of cardiovascular diseases. Abnormal lipid metabolism can lead to the formation of atherosclerotic plaque, which eventually leads to arterial stenosis and vascular occlusion. In addition, high triglyceride levels are also associated with increased cardiovascular risk. Abnormal lipid metabolism may also trigger chronic inflammatory reaction and aggravate the development of atherosclerosis.
Vascular smooth muscle cells (VSMCs) are a specialized type of muscle cells located within the blood vessel walls. They play a crucial role in vascular function by regulating the diameter of blood vessels, controlling blood flow, and blood pressure. VSMCs do not undergo terminal differentiation and can undergo phenotypic changes under pathological conditions, which are closely associated with various cardiovascular diseases such as stroke, atherosclerosis, myocardial infarction, and peripheral arterial diseases. Common protein markers for vascular smooth muscle cells include ACTA2, CNN1, TAGLN, and TAGLN2.
Cardiac stem cells (CSCs) are considered to be a quiescent population of cells residing in the heart tissue, capable of self-renewal in vitro. During cell division, these cells can multiply in number through symmetric division. Alternatively, these stem cells can undergo asymmetric cell division, giving rise to daughter stem cells and progenitor cells. The latter can differentiate into three main types of cardiac cells: cardiomyocytes, endothelial cells, and smooth muscle cells. Cardiac stem cells have specific protein cell markers. Common CSC markers include c-kit, ISL1, ABCG2, BMP4, ACTA2, and NPPA, among others.
Cardiomyocytes are cells that constitute the cardiac muscle tissue, responsible for the contraction and pumping function of the heart. Unlike skeletal muscle cells, cardiomyocytes are non-renewable cells. They have intrinsic contractile properties, allowing them to contract autonomously without external stimulation. Cardiomyocytes possess excitability, conductivity, and automaticity, making them essential targets for researching and developing drugs to treat heart muscle diseases by influencing their functional characteristics.
Endothelial cells (ECs) are flat, elongated cells that form a single-cell-thick layer covering the inner lining of blood vessels, known as the endothelium. They are a major component of the blood vessel wall, along with smooth muscle cells and the basement membrane, forming the fundamental structure of blood vessels. Endothelial cells have various crucial functions, including maintaining the normal physiological state of blood vessels, controlling vascular permeability, regulating blood pressure, promoting blood flow, and inhibiting the coagulation process. Endothelial cells are characterized by specific protein cell markers, which range from receptor tyrosine kinases, such as VEGFR, to cell adhesion proteins, such as ICAM1.
Code | Product Name | Sensitivity | Target |
---|---|---|---|
CSB-E11269h | Human Angiotensin Ⅰ Converting Enzyme,ACEⅠ ELISA Kit | 4.7 pg/mL | ACE |
CSB-E04492m | Mouse Angiotensin converting enzyme,ACE ELISA Kit | 0.39 ng/mL | ACE |
CSB-E04490r | Rat Angiotensin converting enzyme,ACE ELISA Kit | 7.81 ng/ml | ACE |
CSB-E04489h | Human Angiotensin converting enzyme 2, ACE2 ELISA Kit | 0.039 ng/mL | ACE2 |
CSB-E17204m | Mouse Angiotensin converting enzyme 2(ACE2)ELISA Kit | 1.56 pg/mL | ACE2 |
CSB-E14308r | Rat Angiotensin converting enzyme 2, ACE2 ELISA Kit | 0.02 ng/ml | ACE2 |
CSB-E09343h | Human α-Smooth muscle actin,α-SMA ELISA Kit | 0.78 ng/mL | ACTA2 |
CSB-EL001366HA | Hamster adiponectin, C1Q and collagen domain containing (ADIPOQ)ELISA kit | 0.117 ng/mL | ADIPOQ |
CSB-EL001371MO | Mouse ADM2(ADM2) ELISA kit | 15.6 pg/mL | ADM2 |
CSB-E07272m | Mouse adiponectin,ADP ELISA Kit | 0.039 ng/mL | ADP |
CSB-E07271r | Rat adiponectin,ADP ELISA Kit | 0.039 ng/mL | ADP |
CSB-E07270h | Human adiponectin,ADP ELISA Kit | 1.102 ng/mL | ADP |
CSB-EL001366Mk | Monkey adiponectin (ADP) ELISA kit | 0.11 ng/mL | ADP |
CSB-E08564h | Human angiotensinogen (aGT) ELISA Kit | 19.5 pg/mL | AGT |
CSB-E11179r | Rat aldehyde dehydrogenase,ALDH ELISA Kit | 0.078 ng/mL | ALDH2 |
CSB-E04498h | Human Angiogenin,ANG ELISA Kit | 3.9 pg/mL | ANG |
CSB-EL001703PI | Pig Angiogenin(ANG) ELISA kit | 47 pg/mL | ANG |
CSB-E08527h | Human angiotensin Ⅰ,Ang-Ⅰ ELISA Kit | 3.9 pg/mL | Ang-Ⅰ |
CSB-E04494r | Rat angiotensin II (ANG-Ⅱ) ELISA kit | 1.17 pg/mL | ANG-Ⅱ |
CSB-E04495m | Mouse angiotensin Ⅱ(ANG-Ⅱ) ELISA Kit | 0.11 pg/mL | ANG-Ⅱ |