Smooth muscle cell-specific haploinsufficiency restricts the progression of abdominal aortic aneurysm by modulating CTGF expression

Keyphrases

• Smooth muscle Cells 100%
• Ruptured Abdominal Aortic Aneurysm (rAAA) 100%
• Haploinsufficiency 100%
• Notch1 100%
• Connective Tissue Growth Factor 100%
• ApoE KO Mice 40%
• Abdominal Aorta 30%
• Aorta 20%
• Cre-Lox Technology 10%
• Immunostaining 10%
• Mouse Model 10%
• Apoptosis 10%
• In Vitro Study 10%
• Macrophages 10%
• Myeloid Cells 10%
• Angiotensin II (Ang II) 10%
• Inflammation 10%
• Infiltration 10%
• Decreased Expression 10%
• Aneurysm Formation 10%
• ApoE 10%
• Associated Proteins 10%
• Per Se 10%
• Dominant Negative 10%
• Small Interfering RNA (siRNA) 10%
• Plasmid 10%
• Cell Culture Model 10%
• Vascular Smooth muscle Cells 10%
• Haploinsufficient 10%
• Matrix-based 10%
• Matrix Remodeling 10%
• In Vitro Cell Culture 10%
• Aneurysm Development 10%
• Notch Intracellular Domain 10%
• Adventitial 10%
• NOTCH3 10%
• Vascular Smooth muscle Cell Phenotype 10%
• Aortic Remodeling 10%
• Mastermind 10%
• Elastin Degradation 10%
• Histoarchitecture 10%
• Phenotype Markers 10%
• Ctgf 10%

Immunology and Microbiology

• Smooth Muscle Cell 100%
• Haploinsufficiency 100%
• Apolipoprotein E Knockout Mouse 100%
• Connective Tissue Growth Factor 100%
• Abdominal Aorta 75%
• Vascular Smooth Muscle Cell 50%
• In Vitro 50%
• Mouse Model 25%
• Macrophage 25%
• Myeloid 25%
• Plasmid 25%
• Cell Culture 25%
• Immunostaining 25%
• Programmed Cell Death 25%
• Angiotensin 25%