Worming along in amyloid cardiotoxicity.

In this issue of Blood, Diomede and colleagues establish a novel Caenorhabditis elegans model of primary amyloid cardiotoxicity. Using pharyngeal pumping as a surrogate for cardiac function, they find that human amyloidogenic light-chain proteins directly impair pharyngeal activity. Direct toxicity was associated with the release of reactive oxygen species, and pharyngeal activity was restored with use of antioxidant agents.