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MicroRNA That Controls Blood Vessel Development Identified

An Indian-origin researcher in the U.S. has announced the identification of a key regulatory factor that controls development of the human vascular system-the extensive network of

A key regulatory factor that controls development of the human vascular system-the extensive network of arteries, veins, and capillaries that allow blood to reach all tissues and organs has been identified by an Indian-origin researcher.

Dr. Deepak Srivastava, the Director of the Gladstone Institute of Cardiovascular Disease (GICD), says that this advancement by researchers from the Gladstone Institute of Cardiovascular Disease (GICD) and UCSF attains significance because it may offer clues to potential therapeutic targets for diseases like heart disease or cancer, which are impacted by or affect the vascular system.

Working with colleagues from the University of California, San Francisco (UCSF), he has discovered that microRNA (miR-126), a tiny RNA molecule, is intimately involved in the response of blood vessels to angiogenic signals.

A research article in the journal Developmental Cell describes Angiogenesis as the process of vascular development.

A cascade of genes orchestrate a series of events leading to formation of blood vessels in an embryo.

"Some of these same gene regulatory networks are re-activated in the adult to direct the growth of new blood vessels. This can be beneficial, as in the case of a heart attack," said Dr. Jason Fish, lead author of the study.

The researcher further said that blood vessel formation could also contribute to disease in settings like cancer, where vessels feed a growing tumour.

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"Finding that a single factor regulates a large part of the angiogenic process creates a significant target for therapeutic development for any disease involving the vascular system," said Dr. Srivastava.

"The next step is to find ways to modify this microRNA in the setting of disease and test its ability to alter the disease process," he added.

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Source-ANI
RAS/L


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