New Drug Class Offers Hope for Calcified Blood Vessels

MedicalResearch.com Interview with:

Dr Mattias Ivarsson PhD CEO, Inositec, co-author of data  

Dr. Ivarsson

Dr Mattias Ivarsson PhD
CEO, Inositec, co-author of data

MedicalResearch.com: What is the background for this study?

Response: When control of factors in the blood that regulate mineral balance in the body is lost, the subsequent build-up of calcium deposits in the arterial walls and cardiac valves lead to an increase in cardiac events, particularly in patients with chronic kidney disease or diabetes, as well as all-cause mortality.

There is a significant unmet need for therapeutic agents capable of reducing pathological mineral accumulation regardless of their root cause. To date, there is no approved therapy for treating calcification-dependent cardiovascular disease.  Continue reading

Genetic Calcification Disorder May Lead To Better Treatment of Atherosclerosis

MedicalResearch.com Interview with:

Manfred Boehm M.D. Senior Investigator Laboratory of Cardiovascular Regenerative Medicine Center for Molecular Medicine NHLBI-NIH Bethesda, MD 20892

Dr. Manfred Boehm

Manfred Boehm M.D.
Senior Investigator
Laboratory of Cardiovascular Regenerative Medicine
Center for Molecular Medicine
NHLBI-NIH
Bethesda, MD 20892

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Common atherosclerosis (hardening of blood vessels) is the leading cause for vascular diseases worldwide. Vascular calcification is a critical component of atherosclerosis and an indicator of negative outcomes. This process is highly regulated and dynamic. However, the underlying mechanism is poorly understood and no direct treatment is available to stop or reverse this devastating buildup of calcium crystals in the vessel wall. Arterial calcification due to deficiency of CD73 is a rare inherited vascular disease characterized by extensive calcification of blood vessels caused by mutation in a gene encoding an enzyme that generates a compound called Adenosine outside of cells. The lack of this important enzyme, CD73, activates a compensatory mechanism to generated Adenosine by an alternative enzyme. Unfortunately, increased activity of this other enzyme is causing accelerated vascular calcification. By using the patient’s own cells, this study characterized the compensatory signaling pathway and discovered several new treatment strategies.

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