Genomes and Genes


William E Louch


Affiliation: University of Oslo
Country: Norway


  1. Louch W, Sejersted O, Swift F. There goes the neighborhood: pathological alterations in T-tubule morphology and consequences for cardiomyocyte Ca2+ handling. J Biomed Biotechnol. 2010;2010:503906 pubmed publisher
    ..Based on this evidence, we propose that T-tubules have the potential to serve as novel therapeutic targets. ..
  2. Louch W, Hake J, Jølle G, Mørk H, Sjaastad I, Lines G, et al. Control of Ca2+ release by action potential configuration in normal and failing murine cardiomyocytes. Biophys J. 2010;99:1377-86 pubmed publisher
    ..Thus, dyssynchronous Ca(2+) release in failing mouse myocytes does not result from electrical remodeling, but rather other alterations such as T-tubule reorganization. ..
  3. Louch W, Stokke M, Sjaastad I, Christensen G, Sejersted O. No rest for the weary: diastolic calcium homeostasis in the normal and failing myocardium. Physiology (Bethesda). 2012;27:308-23 pubmed publisher
    ..These discussions illustrate that the diastolic phase is not simply a period of rest but rather involves highly regulated and dynamic Ca(2+) fluxes. ..
  4. Roe A, Frisk M, Louch W. Targeting cardiomyocyte Ca2+ homeostasis in heart failure. Curr Pharm Des. 2015;21:431-48 pubmed
    ..We discuss experimental data indicating the applicability of these targets that has led to recent and ongoing clinical trials, and suggest future therapeutic approaches. ..
  5. request reprint
    Hodne K, Lipsett D, Louch W. Gene Transfer in Isolated Adult Cardiomyocytes. Methods Mol Biol. 2017;1521:169-182 pubmed
    ..Included are detailed protocols for isolating cells, maintaining rod shaped cardiomyocytes in culture over several days, and employing adenovirus for gene transduction. ..
  6. Louch W, Hougen K, Mørk H, Swift F, Aronsen J, Sjaastad I, et al. Sodium accumulation promotes diastolic dysfunction in end-stage heart failure following Serca2 knockout. J Physiol. 2010;588:465-78 pubmed publisher
    ..Our observations indicate that if cytosolic Na(+) gain is prevented, up-regulated Ca(2+) extrusion mechanisms can maintain near-normal diastolic function in the absence of SERCA2. ..