This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
, No Gclids
Disease Info Card
Tricuspid Valve Insufficiency
Information about Tricuspid Valve Insufficiency: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.
Overview of Tricuspid Valve Insufficiency
Most recent studies have shown that Tricuspid Valve Insufficiency shares some biological mechanisms with aortic-valve-insufficiency, atrial-fibrillation, cardiac-arrhythmia, congenital-heart-defects, endocarditis, heart-diseases, heart-failure, heart-septal-defects, heart-valve-disease, hypertensive-disease, mitral-valve-insufficiency, mitral-valve-stenosis, pathological-dilatation, pulmonary-hypertension, pulmonary-valve-insufficiency, regurgitation, rheumatic-heart-disease, stenosis, tricuspid-valve-stenosis, ventricular-septal-defects.
Among the many pathways, these few ones have gauged particular interests from scientists studying Tricuspid Valve Insufficiency, and have been seen in publications frequently: Aging, Cell Adhesion, Cell Proliferation, Coagulation, Dehiscence, Delamination, Diuresis, Excretion, Glomerular Filtration, Hemostasis, Inflammatory Response, Localization, Pathogenesis, Platelet Aggregation, Secretion, Segmentation, Transport, Transposition, Vasoconstriction, Vasodilation
Quite a number of genes have been found to play important roles in Tricuspid Valve Insufficiency, such as AMY2A, ASAP1, ASAP2, BLOC1S6, CPB1, F2R, MRPS30, PAPOLA, PDAP1, PRH1, REG3A, TFRC, TMEFF2, TUSC2, TXNRD1, TXNRD2. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.
In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.