The mice hearts worked better and had stronger beats. In subsequent work, he and co-workers used gene therapy to restore S100A1 levels – and heart function – to normal in failing animal hearts.
Congestive heart failure affects nearly five million Americans, many of whom have poor long-term prognoses, despite recent therapeutic advances.
In the study, the researchers caused simulated heart attacks in the two groups of animals.
"At the basal level, hearts from S100A1 knockouts don't appear to be that different," says Dr. Koch, who is W.W. Smith Professor of Medicine at Jefferson Medical College. Yet, when they caused a heart attack, "the hearts basically fell apart," he says, adding, "S100A1 appears to be a critical molecule to the adaptation of the heart to stress."
Generally, mice survive heart attacks but within a few weeks go on to develop heart failure, he notes. But without S100A1, the researchers found a more rapid onset of heart failure, which includes a higher rate of heart cell death.
The scientists compared these results to the mice with increased levels of S100A1 in the heart who also had an occluded artery and a simulated heart attack. They found the opposite effects in these mice. In fact, the hearts of these mice appeared stronger than normal mice, and did not go on to develop heart failure during the next 20 days.
"It's clear that S100A1 expression goes down after a heart attack, which is consistent with what we've seen in the past in knockouts, and the transgenic mice never lose anything," Dr. Koch says.
According to Dr. Koch, while he and his co-workers will continue to pursue new strategies using gene therapy to manipulate S100A1 levels for treating heart failure, he notes that the current study also provides insights into the potential mechanisms behind the observed S100A1 effects. They have demonstrated a newly discovered link between a certain molecular signaling pathway and changes in S100A1 lePage: 1 2 3 Related medicine news :1
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