Cardiotrophin 1 Spurs Greater Regeneration Following Heart Injury

Researchers have in recent years found a number of ways to enhance regeneration in specific tissues in various laboratory species. In this one the focus is on cardiotrophin 1, and is particularly interesting when held up in comparison to what is known of the roles and relationships in heart aging from other studies of this gene. Here, researchers temporarily increase cardiotrophin 1 levels in rodents in order to produce improved regeneration of damaged heart tissue in a scenario of heart failure. Yet in the past, it was demonstrated that cardiotrophin 1 knockout mice, lacking this protein throughout their lives, live longer than their unmodified peers. This is thought to be the case because this protein spurs greater arterial stiffness and fibrosis of heart tissue, as well as greater hypertrophy as heart muscle enlarges in response to rising blood pressure and other changes that accompany aging. This hypertrophy isn't beneficial: it is a form of dysfunction, a structural alteration that weakens the heart and disarrays normal processes in ways that can lead to heart failure. How to reconcile these opposing observations? Perhaps by looking at the way in which regeneration runs awry in old age: regenerative processes are disrupted by inflammation resulting from senescent cells and immune system failure. Fibrosis is one of the consequences, the generation of scar-like structures in place of correctly functioning tissue. Everything else being equal, more active regeneration...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs