Mitochondrial Dysfunction as a Cause of Atrial Fibrillation

For any given age-related condition, you will find papers in the literature that focus on one mechanism of aging and its contribution to that condition. Usually these are reviews covering the details of the mechanism and how it causes pathology, or the epidemiology of the mechanism in the field, as absent an effective means of intervention it is very challenging to establish just how large a contribution that mechanism actually has. While looking through the work here on age-related mitochondrial dysfunction and atrial fibrillation, it is worth also taking a look at past work on senescent cell burden as a cause of atrial fibrillation, potentially via inflammatory, pro-growth signaling that leads to fibrosis in heart tissue. In both cases there are approaches to addressing the issue, mitochondrial replacement and senolytic drugs to destroy senescent cells, but those assessments have yet to be carried out rigorously. Until they have one, there is no way to predict which of these contributing causes is more or less important than the other. Atrial fibrillation (AF) is the most common cardiac arrhythmia and contributes to a high prevalence of mortality and morbidity. The shortening of telomere length has been found to be common with age. Research efforts have argued that leukocyte telomere length (LTL) shortening is related to a variety of cardiovascular diseases, including atherosclerosis, left ventricular hypertrophy, and heart failure, but the relevance to AF i...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs