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Tenascin-C may accelerate cardiac fibrosis by activating macrophages via the integrin αVβ3/nuclear

Naoshi Shimojo1, Ryotaro Hashizume2, Kazuki Kanayama2

  • 1From the Department of Pathology and Matrix Biology (N.S., R.H., M.H., Y.S., T.N., M.H., T.Y., K.I.-Y.), and Department of Pathologic Oncology (K.K.), Mie University Graduate School of Medicine, Tsu, Mie, Japan; Mie University Research Center for Matrix Biology, Tsu, Mie, Japan (N.S., R.H., T.Y., K.I.-Y.); and Department of Cardiology, National Center of Global Health and Medicine, Toyama, Shinjuku-ku, Tokyo, Japan (M.H.). nshimojo@doc.medic.mie-u.ac.jp.

Hypertension (Dallas, Tex. : 1979)
|August 5, 2015
PubMed

Keywords:
angiotensin IIcardiac fibrosishypertensionremodelingtenascin-C

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