Cellular Stress Signaling in the Development of Ventricular Fibrillation

Researchers here report on a mechanism by which increased cellular stress in heart tissue can disrupt the regulation of the heartbeat, thus leading to arrhythmia and potentially fibrillation. The accumulated molecular damage of aging, of course, provides increased contributions to cell stress, whether from inflammatory signaling, mitochondrial dysfunction, increased presence of molecular waste, or other causes. When researchers characterize more of the ways in which regulatory pathways in cells can produce maladaptive reactions to this damage, they tend to then search for means to alter the response, rather than means to repair the underlying damage. More focus should go towards damage repair in the research community, but that that is largely not the way in which research and development progresses. Ventricular fibrillation is the most frequent cause of sudden cardiac death. Although aging is an established risk factor for the development of cardiac arrhythmia, the mechanisms underlying this connection have been hard to pin down, hindering progress toward the development of specific treatments. With the development of an arrhythmia, the cardiac cycle speeds up and becomes irregular, with potentially life threatening consequences. Working with animal models, researchers discovered a connection between the development of ventricular fibrillation and the activation of two key signaling proteins, the stress kinases p38γ and p38δ. This discovery opens the way to...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs