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Volume 13 Issue 5, May 2007

Understanding how external stimuli promote muscle growth and maintenance is key to developing therapies for muscular dystrophies. In this issue, Montminy and colleagues identify a molecular mechanism involving CREB by which catecholamines and electrical activity induce myogenesis and muscle repair. The cover image depicts nuclear (dark blue) and cytoplasmic (magenta)staining of HDAC5 in wild-type muscle. Photo courtesy of Rebecca Berdeaux and Marc Montminy.

Volume 13 Issue 5

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Editorial

  • If American science is to meet the needs of all of its citizens, its scientists must reflect the diversity of the country's population.

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News & Views

  • A drug that elevates host cAMP levels forces pathogenic bacteria out of bladder epithelial cells. This process may make urinary tract infections more amenable to treatment with antibiotics (pages 625–630).

    • Danelle S Eto
    • Matthew A Mulvey
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  • Imaging of inflammation in atherosclerotic lesions may identify plaques vulnerable to rupture, and lead to better assessment of individuals at risk for acute coronary events such as myocardial infarction (pages 636–641).

    • Jagat Narula
    • H William Strauss
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  • A single molecule, osteopontin, seems to both amplify and quell the immune response in asthma—depending on the stage of the asthmatic reaction. The findings hint that, if given at the right stage, osteopontin might have value as a therapy (pages 570–578).

    • Mari L Shinohara
    • Harvey Cantor
    News & Views

  • A key regulator of the neuromuscular junction, the transcriptional co-activator PGC-1α, is a potential target for Duchenne muscular dystrophy therapy.

    • Kay E Davies
    • Tejvir S Khurana
    News & Views

  • The presence of autophagic morphology in failing heart muscle cells has suggested that autophagy causes heart failure. Instead, it seems that the opposite is true: autophagy is critical for normal heart function (pages 619–624).

    • Richard N Kitsis
    • Chang-Fu Peng
    • Ana Maria Cuervo
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