
Key PointsThe reduced thrombosis in Klkb1−/− mice is not by defective contact activation. Overexpressed renal Mas with elevated plasma prostacyclin increases aortic Sirt1 and KLF4 and reduces aortic TF protecting Klkb1−/− mice.
Mice, Knockout, Receptor, Bradykinin B2, Angiotensin II, Imidazoles, Kruppel-Like Transcription Factors, Prekallikrein, Nerve Tissue Proteins, Naphthalenes, Epoprostenol, Proto-Oncogene Mas, Peptide Fragments, Receptors, G-Protein-Coupled, Kruppel-Like Factor 4, Mice, Pyrones, Proto-Oncogene Proteins, Animals, Partial Thromboplastin Time, Carotid Artery Thrombosis, RNA, Messenger
Mice, Knockout, Receptor, Bradykinin B2, Angiotensin II, Imidazoles, Kruppel-Like Transcription Factors, Prekallikrein, Nerve Tissue Proteins, Naphthalenes, Epoprostenol, Proto-Oncogene Mas, Peptide Fragments, Receptors, G-Protein-Coupled, Kruppel-Like Factor 4, Mice, Pyrones, Proto-Oncogene Proteins, Animals, Partial Thromboplastin Time, Carotid Artery Thrombosis, RNA, Messenger
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