A research group from the department of medicine at the Universidad Autónoma de Madrid (UAM) has studied the causes and consequences of the cell suicide of renal cells.
Diabetes slowly destroys the kidney up to the point where the renal function has to be taken on by dialysis (artificial kidney) or a transplanted kidney. It is the leading cause of end stage renal failure that requires dialysis. The destruction of the kidney comes from the loss of its cells, which recent studies have demonstrated to be caused by apoptosis, a process that, for cells, involves death by suicide.
Cells suicide when their environment does not “please” them, when their surroundings feel hostile or stressful. The Spanish team managed by Alberto Ortiz, professor of the department of medicine of the UAM based at the Jiménez Díaz-Capio foundation, has spent years studying the causes and the consequences of kidney cell suicide, specializing in “psycho-cellulology”.
The team analyzed the genes related with apoptosis as a part of a European collaborative effort (European Renal Biopsy Bank) that studies the expression pattern of genes found in patients suffering from diabetic nephropathy. The affected kidneys exhibited an abnormal expression of 112 genes that regulate the cell suicide. Among these genes, the Spanish team identified a protein of the Tumour Necrosis Factor (TNF) family, called TRAIL, as the key to the cell suicide in diabetes affected kidneys.
In these kidneys, large quantities of TRAIL can be found that surprisingly do not come from the increased glucose levels that define the disease, but from the inflammation that accompanies the renal damage. Inflammation and higher glucose levels favour renal damage; the inflammation raises the TRAIL levels while the hyperglycaemia generates a stressful environment that, in the presence of TRAIL, leads to cell suicide.
The role played by inflammation in the cell suicide that leads to renal damage suggests that the treatment of diabetic nephropathies requires a multiple attack to control the glucose levels while also acting on the renal inflammation and lethal proteins like TRAIL.
This study is part of the efforts carried out by the Red de Investigación Renal (RedInRen), financed by the Carlos III institute, to expose the mechanisms of renal lesions and develop new treatments for renal diseases. The results from this study have been published on-line in the Journal of the American Society of Nephrology (J Am Soc Nephrol. 2008, [Epub ahead of print]), the most representative journal for Nephrology and Urology.
Oficina de Cultura Científica | alfa
NIH scientists describe potential antibody treatment for multidrug-resistant K. pneumoniae
14.03.2018 | NIH/National Institute of Allergy and Infectious Diseases
Researchers identify key step in viral replication
13.03.2018 | University of Pittsburgh Schools of the Health Sciences
A new scenario seeking to explain how Mars' putative oceans came and went over the last 4 billion years implies that the oceans formed several hundred million...
For the first time, an interdisciplinary team from the University of Basel has succeeded in integrating artificial organelles into the cells of live zebrafish embryos. This innovative approach using artificial organelles as cellular implants offers new potential in treating a range of diseases, as the authors report in an article published in Nature Communications.
In the cells of higher organisms, organelles such as the nucleus or mitochondria perform a range of complex functions necessary for life. In the networks of...
Animal photoreceptors capture light with photopigments. Researchers from the University of Göttingen have now discovered that these photopigments fulfill an...
On 15 March, the AWI research aeroplane Polar 5 will depart for Greenland. Concentrating on the furthest northeast region of the island, an international team...
The world’s second-largest ice shelf was the destination for a Polarstern expedition that ended in Punta Arenas, Chile on 14th March 2018. Oceanographers from...
19.03.2018 | Event News
16.03.2018 | Event News
13.03.2018 | Event News
20.03.2018 | Physics and Astronomy
20.03.2018 | Physics and Astronomy
20.03.2018 | Earth Sciences