Thus, we provide novel insights into the role of Akt1-mediated β-catenin signaling in EndMT and pathological vascular remodeling, and present β-catenin as a potential target for therapy for various cardiopulmonary diseases involving vascular remodeling.
The present review analyzes and summarizes the patent literature regarding human neutrophil elastase inhibitors for the treatment of cardiopulmonary diseases over 2014-2018.
Accordingly, DB is often underdiagnosed or misdiagnosed, given the similarity of its associated symptoms (dyspnea, tachycardia, and dizziness) to those of other common cardiopulmonary diseases such as COPD and asthma.
IL-6 and CRP are correlated with the onset of PHD, and there are also correlations between the polymorphisms of IL-6 rs1800796 and CRP rs2794521 and the disease.
Thus, we provide novel insights into the role of Akt1-mediated β-catenin signaling in EndMT and pathological vascular remodeling, and present β-catenin as a potential target for therapy for various cardiopulmonary diseases involving vascular remodeling.
IL-6 and CRP are correlated with the onset of PHD, and there are also correlations between the polymorphisms of IL-6 rs1800796 and CRP rs2794521 and the disease.
Here, we hypothesize that engraftment of healthy BM to <i>CAV-1</i> KO mice will prevent pulmonary vascular remodeling and development of the cardiopulmonary disease.
Here, we hypothesize that engraftment of healthy BM to <i>CAV-1</i> KO mice will prevent pulmonary vascular remodeling and development of the cardiopulmonary disease.
Here, we hypothesize that engraftment of healthy BM to <i>CAV-1</i> KO mice will prevent pulmonary vascular remodeling and development of the cardiopulmonary disease.
Upregulation of the ACE/Ang II/AT1R axis shifts the system toward vasoconstriction, proliferation, hypertrophy, inflammation, and fibrosis, all factors that contribute to the development and progression of cardiopulmonary diseases.
Upregulation of the ACE/Ang II/AT1R axis shifts the system toward vasoconstriction, proliferation, hypertrophy, inflammation, and fibrosis, all factors that contribute to the development and progression of cardiopulmonary diseases.
Upregulation of the ACE/Ang II/AT1R axis shifts the system toward vasoconstriction, proliferation, hypertrophy, inflammation, and fibrosis, all factors that contribute to the development and progression of cardiopulmonary diseases.
Intracellular processing of endothelial nitric oxide synthase isoforms associated with differences in severity of cardiopulmonary diseases: cleavage of proteins with aspartate vs. glutamate at position 298.