What they say:
A study from the University of California, La Jolla, California, USA shows that “Notch3 signaling promotes the development of pulmonary arterial hypertension.” This study was published in the 15 November 2009 issue of the journal “Nature Medicine”[the number 1 journal in General Medicine with an I.F of 28.054] by Prof. Thistlethwaite PA, Li X and others.
What we say:
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for pulmonary arterial hypertension: Azilsartan[Brand name: Edarbi], an angiotensin II type 1 receptor blocker used in the treatment of high blood pressure, inhibits the development of pulmonary arterial hypertension via down regulation of its target gene Notch3
Significance of the study:
Azilsartan, by increasing the expression of its target gene, it may decrease the expression of Notch3 and its target gene Hes-5 (Fig.1).
Figure 1. Mechanistic insights into how Azilsartan inhibits the development of pulmonary hypertension via up regulation of its target gene
Figure 2. The chemical structure of Azilsartan.
Thus, pharmacological formulations encompassing “Azilsartan or its analogues, either alone or in combination with other drugs,“ may be used to treat pulmonary arterial hypertension.
Details of the research findings:
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
Undisclosed mechanistic information: How Azilsartan decreases the expression of Notch3
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References:
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Citation: Boominathan, L., Molecular therapy for pulmonary arterial hypertension: Azilsartan[Brand name: Edarbi], an angiotensin II type 1 receptor blocker used in the treatment of high blood pressure, commonly used in the treatment of heart failure and arrhythmias, inhibits the development of pulmonary arterial hypertension via down regulation of its target gene Notch3, 28/December/2017, 12.45 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
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