Diabetics are more at risk to develop kidney failure. Especially in case of tubular autophagy. The University of Augsburg is issuing the following study on how these two diseases are linked in diabetics.

Researchers at the University of Augsburg, Bavaria (Germany), believe they have demonstrated one of the mechanisms underlying the weakening of kidney cleansing activity in the diabetics. An important discovery, which foreshadows improvement in pharmacological treatments in this area. According to the chief researcher, it is conceivable a slowdown in the development of diabetes of 20 or 30 years.

30-40% of diabetics tend to develop mechanisms of the slow failure of the kidney.

This study has been published in the Journal of Clinic Investigation. The German researchers explain a good part of it, which can be traced back to the tubular autophagy process.

Tubular autophagy is essentially the process by which the cell gets rid of its waste or recycles it.

The mechanism, just to understand, is considered so relevant that the Karolinska Institutet in Stockholm awarded the pioneer of autophagy research, Yoshinori Ohsumi with the Nobel Prize for Medicine in 2016

The malfunctioning of the autophagic mechanism is believed to be at the basis of diseases such as Sla, Alzheimer’s disease (dementia) and Huntington’s disease, just to name a few.

The diminished ability to activate cleaning mechanisms “leaves the kidneys more vulnerable,” said Toni Baker, director of communications at the university’s medical school.

University of Augsburg satisfaction with this study on tubular autophagy and kidney failure among diabetics 

“This is the first time we have understood that there is a new mechanism that leads to tubular autophagy dysfunction in chronic kidney disease, such as in diabetics,” says Zheng Dong, author of the study and professor of biology and cellular anatomy at the Faculty of Medicine at the University of Augsburg.

New therapies for diabetes:

The researchers noted a dramatic decrease in autophagy activity in the kidneys. This decrease in activity causes a proliferation of diseased kidney cells, which could then lead to urinary tract infections.

To investigate the causes of this dysfunction, the researchers used mice. On them they found a slowdown in autophagy caused by a decrease in levels of the autophagy activation gene (ULK1), which in turn is caused by the microRNA miR-214, which usually does not participate in this process and yet is increased.

This microRNA is in turn controlled by the tumor suppressor (p53), which is known to regulate the cell cycle.

According to the study director, acting with miR-214 would probably make more sense because it clearly seems to inhibit autophagy in diabetes and does not play an obvious role in renal function.

P53, its regulator, is probably not a good target because it limits cell proliferation as a whole.

However, it could offer the therapeutic possibility to better regulate autophagy by increasing its action.

With this research on kidney failure aong diabetics tied to autophagy, “We can delay renal failure for 20 or 30 years or even prevent it in the first place,” said Zheng Dong.

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SOURCE

UNIVERSITY OF AUGSBURG