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Kidney disease vascular calcification of the "culprit" tu

  Recently, Benjamin D. Humphreys of the University of Washington and colleagues reported that they have found stem cells that cause calcification of the blood vessels in chronic kidney disease. This study lays the foundation for further research and development of new therapeutic methods for the treatment of vascular calcification and delaying atherosclerosis. The results are published in the journal Cell Stem Cell.

  Benjamin D. Humphreys says, "In the past we thought that calcification was a passive process - just like the formation of a water pipe wall scale, and later we found that calcification is an active process that is regulated by the cells, Which, from where, has been controversial.

  This study shows that Gli1-positive stem cells are associated with intravascular calcification. Because Gli1-positive stem cells are adult stem cells, Gli1 cells can differentiate into different types of connective tissue, including smooth muscle, fat and bone.

  Humphreys and colleagues found that Gli1 cells can differentiate into smooth muscle cells, restore vasoconstriction, and play an important role in repairing vascular injury after vascular injury. However, patients with chronic kidney disease Gli1 cells may accept a variety of signals, into osteoblasts, leading to calcium deposition.

  "We want osteoblasts to be found only in the bone, not in the blood vessels," says the researchers. "The Gli1 cells of chronic kidney disease can differentiate into osteoblasts that secrete bone matrix in the blood vessel wall, causing calcium deposition." Renal failure Gli1 cells can play a role in repairing spontaneously, but the toxin and inflammatory environment are misleading, and the cells are misinterpreted and transformed into the wrong cell type.

  Researchers also studied tissue in patients with renal failure who died of aortic calcification, and found that Gli1 cells were found in the calcified arteries in the same location as mice.

  According to the US Centers for Disease Control and Prevention reported that about 20 million adults in the United States with varying degrees of chronic kidney disease. However, most patients do not progress to renal failure, dialysis or kidney transplantation, because patients progress to renal failure before the death of cardiovascular disease. Atherosclerosis - a feature of cardiovascular disease - can further aggravate kidney disease.

  The researchers also found that removal of Gli1 cells in mice to prevent calcification formation. The results further support the Gli1 cells are leading to calcification of the "culprit."

  Humphreys said, "Since we have determined that Gli1 cells can cause arterial wall calcium deposition, then you can start to develop drugs that can prevent the process, which will be the main killer of kidney disease - vascular calcification of the new method.But in view of these cells But also has the role of repair of smooth muscle injury, therefore, in the development of new drugs to prevent calcification at the same time should not eliminate its inherent repair.

  Source: Adventitial MSC-like cells are progenitors of vascular smooth muscle cells and drive vascular calcification in chronic kidney disease. Cell Stem Cell. Sept. 8, 2016.

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