The research team is headed by Dr. Rabea Hinkel and Prof. Christian Kupatt, cardiologists at TUM's Klinikum rechts der Isar.
‘Genetic therapy that promotes the production of the molecule thymosin beta 4, stimulates the growth of blood vessels, and reduces the risk of heart attack in diabetics.’
In the research, blood vessels of patients with and without diabetes, undergoing heart transplants, were compared and the samples from diabetics showed significantly reduced numbers of small blood vessels around the heart.
Elevated blood sugar levels are associated with a loss of cells known as pericytes.
"These cells normally form a layer wrapped around the small blood vessels," explains Rabea Hinkel. "We believe that this layer has a stabilizing function. When it is damaged, the entire blood vessel becomes unstable and ultimately breaks up."
When diabetes is left untreated, it causes steady decrease in capillary density around the heart. This has been confirmed by animal experiments.
"Diabetes often remains undetected in patients for years or even decades. Over that long period, massive damage can occur," says Rabea Hinkel.
Genetic Therapy
Though the loss of capillaries is not irreversible, the research team applied a genetic therapy to stimulate heart cells, to increase production of the molecule thymosin beta 4. This protein stimulates the growth of pericytes.
The growth of pericytes induces the growth of lasting and functional capillary networks.
"It will be a while before this kind of therapy can be used in humans," says Christian Kupatt. "But we were able to show for the first time in a transgenic large animal model, which closely models human type I diabetes mellitus, how diabetes damages the heart. That opens up new perspectives for treating patients. It also further reinforces our awareness of how important it is to diagnose diabetes early."
The results are published in the
Journal of the American College of Cardiology.
Reference
- Rabea Hinkel et al. Diabetes Mellitus-Induced Microvascular Destabilization in the Myocardium. Journal of the American College of Cardiology; (2017) DOI: 10.1016/j.jacc.2016.10.058.
Source: Medindia