Loss of Bmx nonreceptor tyrosine kinase prevents pressure overload-induced cardiac hypertrophy.

Journal Article (Journal Article)

Bmx nonreceptor tyrosine kinase has an established role in endothelial and lymphocyte signaling; however, its role in the heart is unknown. To determine whether Bmx participates in cardiac growth, we subjected mice deficient in the molecule (Bmx knockout mice) to transverse aortic constriction (TAC). In comparison with wild-type mice, which progressively developed massive hypertrophy following TAC, Bmx knockout mice were resistant to TAC-induced cardiac growth at the organ and cell level. Loss of Bmx preserved cardiac ejection fraction and decreased mortality following TAC. These findings are the first to demonstrate a necessary role for the Tec family of tyrosine kinases in the heart and reveal a novel regulator (Bmx) of pressure overload-induced hypertrophic growth.

Full Text

Duke Authors

Cited Authors

  • Mitchell-Jordan, SA; Holopainen, T; Ren, S; Wang, S; Warburton, S; Zhang, MJ; Alitalo, K; Wang, Y; Vondriska, TM

Published Date

  • December 5, 2008

Published In

Volume / Issue

  • 103 / 12

Start / End Page

  • 1359 - 1362

PubMed ID

  • 18988895

Pubmed Central ID

  • PMC2735252

Electronic International Standard Serial Number (EISSN)

  • 1524-4571

Digital Object Identifier (DOI)

  • 10.1161/CIRCRESAHA.108.186577


  • eng

Conference Location

  • United States