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Vinculin and Talin
  1. Alice Zemljic-Harpf, MD*†,
  2. Ana Maria Manso, PhD*†,
  3. Robert S. Ross, MD*†
  1. From the * Department of Medicine, UCSD School of Medicine, La Jolla; and †Veterans Administration San Diego Healthcare System, San Diego, CA.
  1. Received September 9, 2009, and in revised form October 8, 2009.
  2. Accepted for publication October 8, 2009.
  3. Reprints: Robert S. Ross, MD, Cardiology Section, Veterans Administration San Diego Healthcare System, 111A, 3350 La Jolla Village Dr, San Diego, CA 92161. E-mail: rross{at}
  4. This work was supported by grants to R.S.R. from the Veterans Administration (VA Merit) and the National Institutes of Health (P01 HL066941 and RO1 HL088390), and the symposium was supported in part by a grant from the National Center for Research Resources (R13 RR023236).

Focus on the Myocardium


Cardiomyopathy is a heart muscle disease caused by decreased contractility of the ventricles leading to heart failure and premature death. Multiple conditions like ischemic heart disease (atherosclerosis), hypertension, diabetes, viral infection, alcohol abuse, obesity and genetic mutations can lead to cardiomyopathy. Single gene mutations in sarcomeric proteins, Z-disk-associated proteins, membrane/associated proteins, intermediate filaments, calcium cycle proteins as well as in modifier genes have been linked to cardiomyopathy. Clinical practice guidelines have been formulated by the American Heart Association and the Heart Failure Association of America on how to genetically evaluate patients with cardiomyopathy. To illustrate the concept that alterations in genes cause cardiovascular disease, this review will focus on two membrane-associated proteins, vinculin and talin. We will discuss the general function of vinculin/metavinulin as well as talin1 and talin2, with emphasis on what is understood about their role in the cardiac myocyte and in whole heart.

Key Words
  • vinculin
  • talin
  • costamere
  • intercalated disk
  • mechanotransduction

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