Association Between the Connexin37 Polymorphism and Peripheral Arterial Disease in Subjects With Type 2 Diabetes
- Naoto Katakami, MD, PHD1,
- Ken'ya Sakamoto, MD, PHD1,
- Hideaki Kaneto, MD, PHD1,
- Munehide Matsuhisa, MD, PHD1,
- Ikki Shimizu, MD, PHD2,3,
- Fukashi Ishibashi, MD, PHD4,
- Takeshi Osonoi, MD, PHD5,
- Atsunori Kashiwagi, MD, PHD6,
- Ryuzo Kawamori, MD, PHD7,
- Masatsugu Hori, MD, PHD1 and
- Yoshimitsu Yamasaki, MD, PHD1
- 1Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Osaka, Japan;
- 2Ehime Prefectural Central Hospital, Matsuyama City, Japan;
- 3Ehime Prefectural Imabari Hospital, Imabari, Japan;
- 4Ishibashi Clinics, Hiroshima, Japan;
- 5Naka Kinen Clinics, Naka City, Japan;
- 6Department of Medicine, Shiga University of Medical Science, Otsu City, Japan;
- 7Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, Tokyo, Japan.
- Corresponding author: Naoto Katakami, katakami{at}medone.med.osaka-u.ac.jp
Connexin37 is one of the major connexins expressed in the endothelium, monocytes, and macrophages and plays important roles in atherogenesis (1). The COOH-terminus of this protein is a substrate for specific kinase or protein partners and thereby functions as a regulatory domain (2). Because the C-to-T substitution at nucleotide 1019 in the connexin37 gene causes a proline-to-serine substitution in the regulatory COOH-terminus, and affects its function, this polymorphism is likely associated with the pathogenesis of atherosclerosis. Indeed, this polymorphism has been shown to associate with the risk of coronary artery disease (3). In this study, we investigated whether this polymorphism is associated with an ankle-brachial blood pressure index (ABI), …
