Copper Excess Impedes Blood Vessel Development In Diabetics
Evidence suggests that diabetes can cause copper to "pile up" inside cells, impeding cell function. This, in turn, can create roadblocks towards making new blood vessels and repairing current ones. This occurs as diabetes causes thickening of the blood vessels, making scarring and blood flow worse. Many of the adverse conditions associated with diabetes are due to angiogenesis, the impeded ability of blood vessels to repair or replace themselves.
Diabetes alters the healthy copper balance that typically enables blood vessel formation, says Dr. Tohru Fukai, a vascular biologist and cardiologist at the Medical College of Georgia at Augusta University's Vascular Biology Center. His research is developing treatments that target the copper transporter, ATP7A, that the body uses to ensure proper copper levels in many body functions.
"..in inflammatory diseases such as diabetes, copper levels within cells become excessive."
Fukai and his team are investigating this unhealthy copper excess and its effects through a National Institutes of Health grant for research. Normally, copper resides with ATP7A in a portion of the cell called the Golgi apparatus. Excess copper is transported to the cell membrane by ATP7A for elimination. The team has found that the balance is off in diabetics. There is more copper than ATP7A to transport it.
This leads to blood vessel degeneration as the copper needed for the vessel cells to regenerate or be built is unable to be transported. The team is now studying why ATP7A levels are low in diabetics and what treatments can be had to change that.
The team knows that a certain key, IQGAP1, a scaffold protein involved in signaling and keeping cell contents in their place, is important to vascular growth while vascular endothelial growth factor (VEGF) works with IQGAP1 to make blood vessels, binding it to a key receptor, VEGF receptor 2. In diabetics, VEGF receptor 2 is impaired and the team has found that low levels of ATP7A are responsible for that.
The team is pursuing ways of increasing ATP7A as a way of potentially reversing these problems or heading them off before they start. They hope to find therapies or drug options that could facilitate that.
Source: Eurekalert.org