Does Your Diabetes Put You At Risk Of Bone Marrow Damage?

A new study has shown that the wellbeing of people with diabetes is at risk of a disease in their bone marrow. Microangiopathy affects the small blood vessels, and is known to harm the wellness of diabetics with renal damage, blindness and heart attacks, but this is the first time that this disease has been shown in bone marrow, which is your main source of stem cells and the tissue contained inside your bones.

 

These cells are not only important because they replace old blood cells, but they also play a huge part in repairing your body after acute injuries and heart attacks, and bone marrow stem cells are the most used in regenerative medicine trials to mend hearts damaged by heart attacks. However, as a consequence of microangiopathy, your bone marrow can become starved and therefore less efficient at healing.

 

For the study, led by Professor Paolo Madeddu, Chair of Experimental Cardiovascular Medicine in the School of Clinical Sciences and Bristol Heart Institute at the University of Bristol, the team looked at the effect that diabetes has on bone marrow stem cells and the nurturing of small blood vessels in humans.

 

The results, which were published in the American Heart Association journal Circulation Research, and funded by the British Heart Foundation (BHF), showed that diabetes can cause your marrow to be profoundly remodelled, causing a shortage of stem cells and many of the surrounded vessels can be replaced by fat. This leads to a vicious cycle of further damage to the marrow as sideline vascular complications progress, and could worsen the consequences of peripheral ischaemia.

 

According to Professor Madeddu, ‘Our study draws attention to the bone marrow as a primary target of diabetes-induced damage. The research suggests that the severity of systemic vascular disease has an impact on bone marrow causing a precocious senescence of stem cells. More severe bone marrow pathologies can cause, or contribute to, cardiovascular disease and lead to worse outcomes after a heart attack, through the shortage of vascular regenerative cells. Clinical evidence indicates that achieving a good control of glucose levels is fundamental to prevent vascular complications, but is less effective in correcting microangiopathy. We need to work hard to find new therapies for mending damaged microvessels.’

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