So, what is pulmonary hypertension (PH) is an increase in blood pressure in the pulmonary artery, pulmonary vein, or pulmonary capillaries, together known as the lung vasculature, leading to shortness of breath, dizziness, fainting, and other symptoms, all of which are exacerbated by exertion. Pulmonary hypertension can be a severe disease with a markedly decreased exercise tolerance and heart failure…..
So we need to find where it starts the problem: AT THE VESSELS..AT THE SMOOTH MUSCLE.
1)WHAT REGULATES SMOOTH MUSCLE DIFFERENTIATION, REPAIR AND REMODELING?RESPONSE: MANY PROTEINS AND MOLECULAR PATHWAYS.
2)IS THERE A RELEVANT PROTEIN THAT WE CAN STUDY????
RESPONSE: YES THERE IS, MYOCARDIN.
3) WHAT IS MYOCARDIN?
RESPONSE: MYOCARDIN IS A MASTER REGULATOR OF SMOOTH MUSCLE GENE EXPRESSION AND EXPLAINS HOW SRF (SERUM RESPONSE FACTOR) CONVEYS SMOOTH MUSCLE SPECIFICITY TO ITS TARGET GENES.
What if we could inhibit myocardin in smooth muscle development? It would be easy for us to control PAH…
Jingjing Li and his team at The University of Calgary in Canada (2012 article), showed recently that myostatin can be inhibited by Atorvastatin (ATV), an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, is widely prescribed as a lipid-lowering drug.
So… now, we know that, a cholesterol drug can inhibit smooth muscle proliferation. But is that a role to PAH???? Is aplicable to PAH?
My study will try to focus on Myocardin and Myostatin expression in smooth muscle. Next post, i will descrive how i am thinking to test this two protein expressions….