kt 5823 has been researched along with Marfan Syndrome, Type I in 1 studies
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 0 (0.00) | 18.2507 |
2000's | 0 (0.00) | 29.6817 |
2010's | 0 (0.00) | 24.3611 |
2020's | 1 (100.00) | 2.80 |
Authors | Studies |
---|---|
Alfayate, A; Bonzón-Kulichenko, E; Campanero, MR; De Backer, J; de la Fuente-Alonso, A; Evangelista, A; Forteza, A; Garcia-Izquierdo, E; González-Valdés, I; López-Maderuelo, D; Martín, CE; Martínez-Martínez, S; Méndez-Olivares, MJ; Mingo, S; Muiño-Mosquera, L; Nistal, JF; Redondo, JM; Ruiz-Rodríguez, MJ; Teixido-Tura, G; Toral, M; Vázquez, J | 1 |
1 other study(ies) available for kt 5823 and Marfan Syndrome, Type I
Article | Year |
---|---|
Aortic disease in Marfan syndrome is caused by overactivation of sGC-PRKG signaling by NO.
Topics: Animals; Aorta; Aortic Aneurysm, Thoracic; Biomarkers; Carbazoles; Cyclic GMP; Cyclic GMP-Dependent Protein Kinase Type I; Disease Models, Animal; Female; Fibrillin-1; Gene Knockdown Techniques; Humans; Male; Marfan Syndrome; Mice; Muscle, Smooth, Vascular; Mutation; Myocytes, Smooth Muscle; Nitric Oxide; Nitric Oxide Donors; Primary Cell Culture; Soluble Guanylyl Cyclase; Ultrasonography | 2021 |