Protein could improve recovery from heart attacks
- Date:
- April 11, 2011
- Source:
- Journal of Clinical Investigation
- Summary:
- Angiogenesis is required during embryonic development and wound healing, as well as during disease processes such as tumor growth. The signals that direct angiogensis could represent novel targets for the development of therapies. A new paper reveals that two related proteins -- DKK1 and DKK2 -- play opposite roles in directing angiogenesis. Remarkably, injection of DKK2 improved vascular regeneration in a mouse model of myocardial infarction (heart attack).
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Angiogenesis, the development of new blood vessels, is required during embryonic development and wound healing, as well as during disease processes such as tumor growth. The signals that direct angiogensis are incompletely understood, but could represent novel targets for the development of therapies that promote or inhibit this process.
In a new paper, Young-Guen Kwon and colleagues, of Yonsei University in Seoul, Korea, investigated the role of two related proteins -- DKK1 and DKK2 -- in angiogenesis. These proteins are known to have similar functions in inhibiting a particular cell signaling pathway, but Kwon and colleagues found that they played opposite roles in directing angiogenesis.
Remarkably, they discovered that injection of DKK2 improved vascular regeneration in a mouse model of myocardial infarction (heart attack). The researchers are hopeful that pharmacological manipulation of DKK1 and DKK2 could be used to treat various vascular diseases.
The research appears in the Journal of Clinical Investigation.
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Journal Reference:
- jeong-Ki Min, Hongryeol Park, Hyun-Jung Choi, Yonghak Kim, Bo-Jeong Pyun, Vijayendra Agrawal, Byeong-Wook Song, Jongwook Jeon, Yong-Sun Maeng, Seung-Sik Rho, Sungbo Shim, Jin-Ho Chai, Bon-Kyoung Koo, Hyo Jeong Hong, Chae-Ok Yun, Chulhee Choi, Young-Myoung Kim, Ki-Chul Hwang, Young-Guen Kwon. The WNT antagonist Dickkopf2 promotes angiogenesis in rodent and human endothelial cells. Journal of Clinical Investigation, 2011; DOI: 10.1172/JCI42556
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