Friday, May 17, 2013

Target to Prevent Hardening of Arteries Identified

Sanford-Burnham Medical Research Institute
Science Daily
May 16, 2013

Summary:
The scientists at Sanford-Burnham Medical Research Institute have been studying the hardening of the arteries. They particularly focused on a destructive protein called Dkk1. Their studies suggest that the development of drug therapies to inhibit Dkk1 signaling may help limit arteriosclerotic disease. This would be helpful for diseases such as chronic renal deficiency or diabetes. In chronic renal deficiency and diabetes, unregulated Dkk1 signaling can be destructive, so restraining the action of Dkk1 for a prolonged period of time may be helpful.

When Dkk1 is working normally, it is essential for wound repair. However, inflammatory responses inside artery walls triggered by hyperglycemia and other metabolic injuries, can trigger prolonged and destructive Dkk1 signaling. Dkk1 causes the conversion of endothelial cells, cells that line the interior surface of artery walls, into mesenchymal cells. It directs connective tissue formation; the process is  called endothelial-mesenchymal transition. The fibrosis inside artery walls that results from this causes a dangerous hardening of arteries that increases blood pressure and ultimately impairs blood flow.

Drug therapy will target specifically where Dkk1 must be inhibited, the arteries. Researchers hope to develop a therapeutic drug that would include a Dkk1 inhibitor and a peptide engineered to target specific vascular tissues. The scientists will continue to research the prevention of artery hardening.

Connection:
This article relates to our study of human body systems because we studied the circulatory systems. The hardening of the arteries is often associated with the disease that we studied, arteriosclerosis. Arteriosclerosis is an advanced stage of plaque buildup in the arteries. The deposits on the artery wall harden. With arteriosclerosis, the arteries lose their ability to stretch. This disease increases blood pressure and the chance for blood clots to form within blood vessels.

5 comments:

  1. How can the inflammatory response triggered by hyperglycemia and other metabolic injuries trigger prolonged and destructive Dkk1 signaling?

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    Replies
    1. Since the function of Dkk1 is wound repair, Dkk1 would be triggered to aid inflammation. This inflammation can be caused by hyperglycemia.
      http://www.sciencedaily.com/releases/2013/05/130516161700.htm

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  2. Are there any negative consequences of inhibiting Dkk1 production?

    ReplyDelete
    Replies
    1. Scientists are trying to develop a therapeutic drug that will specifically target the malfunctioning Dkk1 (the Dkk1 in the arteries). There would be negative consequences for inhibiting ALL Dkk1 because there is healthy Dkk1 regulating cartilage and joint remodeling. However, scientists are trying to devise a method to only inhibit malfunctioning Dkk1 in the arteries.
      http://www.sciencedaily.com/releases/2013/05/130516161700.htm

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  3. This comment has been removed by the author.

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