Arguing for Raised O-GlcNAcylation to be Closer to the Cause of Heart Failure than Thought

Researchers here use animal models to argue that raised levels of O-GlcNAcylation observed in heart failure patients are more important than thought as a contributing cause to the progression of this condition, rather than being further downstream as an end consequence. One must always be careful, however, in analysis of work where researchers break some important mechanism, causing problems, and then fix it. It is always possible to produce harm by causing unnatural disarray to a specific mechanism in animal metabolism. Removing that unnatural disarray will always help. That doesn't mean that the model necessarily has relevance to a condition in which the specific mechanism appears - relevance strongly depends on the specific details. Proteins within living cells can be modified with the addition of small chemical groups that coax the proteins to change their shape or function. Among those modifications is O-GlcNAcylation, the addition of the sugar molecule O-GlcNAc (O-linked N-acetylglucosamine). The modification is controlled by two other molecules: O-GlcNAc transferase (OGT), an enzyme that adds the sugars to proteins, and O-GlcNAcase (OGA), an enzyme that facilitates their removal. Researchers have long known that proteins in the cells of people with heart failure have more O-GlcNAc than usual. But whether increased levels of the sugar were a cause or consequence of heart failure - or an attempt by the body to ward off heart failure - has been unclear. Re...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs