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Research with mice and rats in Germany may have found a new way to treat high blood pressure.
Using epifluorescence intravital video microscopy imaging, researchers examined mice to whom they had given angiotensin II hormones to induce arterial hypertension.
They determined that the mice with low levels of thrombin-driven factor XI (FXI) – either naturally or inhibited by antisense oligonucleotides – had healthier endothelium.
“Specificity of the effects of FXI depletion was confirmed by continuous in vivo supplementation with human FXI,” wrote Sabine Kossmann, PhD, of the Center for Thrombosis and Hemostasis, University Medical Center, Mainz (Germany), and her coauthors (Sci Transl Med. 2017 Feb 1. doi: 10.1126/scitranslmed.aah4923).
Targeting the “feedback loop” between the FXI and a receptor that helps thrombin propagate on platelets reduced both vascular inflammation and blood pressure.
“Our findings suggest that inhibiting the ... thrombin-FXI–amplifying loop may provide added cardiovascular benefits that are synergistic with those of established platelet inhibitors,” the authors wrote.
This work was supported by grants from the Stiftung Pathobiochemie und Molekulare Diagnostik and the Federal Ministry of Education and Research. The authors disclosed funding and grants from the German Research Society, the European Research Council, NIH, and other sources. One of the researchers is inventor of five patents related to the FXI inhibitor and equity holder in Aronora, and may have financial interest in the findings of the research.
Research with mice and rats in Germany may have found a new way to treat high blood pressure.
Using epifluorescence intravital video microscopy imaging, researchers examined mice to whom they had given angiotensin II hormones to induce arterial hypertension.
They determined that the mice with low levels of thrombin-driven factor XI (FXI) – either naturally or inhibited by antisense oligonucleotides – had healthier endothelium.
“Specificity of the effects of FXI depletion was confirmed by continuous in vivo supplementation with human FXI,” wrote Sabine Kossmann, PhD, of the Center for Thrombosis and Hemostasis, University Medical Center, Mainz (Germany), and her coauthors (Sci Transl Med. 2017 Feb 1. doi: 10.1126/scitranslmed.aah4923).
Targeting the “feedback loop” between the FXI and a receptor that helps thrombin propagate on platelets reduced both vascular inflammation and blood pressure.
“Our findings suggest that inhibiting the ... thrombin-FXI–amplifying loop may provide added cardiovascular benefits that are synergistic with those of established platelet inhibitors,” the authors wrote.
This work was supported by grants from the Stiftung Pathobiochemie und Molekulare Diagnostik and the Federal Ministry of Education and Research. The authors disclosed funding and grants from the German Research Society, the European Research Council, NIH, and other sources. One of the researchers is inventor of five patents related to the FXI inhibitor and equity holder in Aronora, and may have financial interest in the findings of the research.
Research with mice and rats in Germany may have found a new way to treat high blood pressure.
Using epifluorescence intravital video microscopy imaging, researchers examined mice to whom they had given angiotensin II hormones to induce arterial hypertension.
They determined that the mice with low levels of thrombin-driven factor XI (FXI) – either naturally or inhibited by antisense oligonucleotides – had healthier endothelium.
“Specificity of the effects of FXI depletion was confirmed by continuous in vivo supplementation with human FXI,” wrote Sabine Kossmann, PhD, of the Center for Thrombosis and Hemostasis, University Medical Center, Mainz (Germany), and her coauthors (Sci Transl Med. 2017 Feb 1. doi: 10.1126/scitranslmed.aah4923).
Targeting the “feedback loop” between the FXI and a receptor that helps thrombin propagate on platelets reduced both vascular inflammation and blood pressure.
“Our findings suggest that inhibiting the ... thrombin-FXI–amplifying loop may provide added cardiovascular benefits that are synergistic with those of established platelet inhibitors,” the authors wrote.
This work was supported by grants from the Stiftung Pathobiochemie und Molekulare Diagnostik and the Federal Ministry of Education and Research. The authors disclosed funding and grants from the German Research Society, the European Research Council, NIH, and other sources. One of the researchers is inventor of five patents related to the FXI inhibitor and equity holder in Aronora, and may have financial interest in the findings of the research.
FROM SCIENCE TRANSLATIONAL MEDICINE