The hidden bowel molecule was found to destroy the kidneys

After finding high levels of Corcine – the small peptide that results Cluster Bacteria in the intestine – in the blood of patients with diabetic kidney fibrosis, the researchers used computer simulation, tissue and mouse experiences to follow how the koricin affects the kidneys, how it reaches there from the intestine, and a possible way to counter the treatment of antibodies.

“Our previous studies have shown that the Kurisians could harm cells and get worse for tissues and fibrosis in other organs, so it may be suspected that he might be a hidden driver for kidney fibrosis,” said Illinois Professor in Illinois. Cann and Gabazza were subsidiaries of the Karl R. And wez for genetic biology in Illinois. “Our new results indicate that Corissin is actually a hidden reason behind gradual kidney damage in diabetes, and that its ban may provide a new way to protect kidney health in patients.”

The researchers published their results in the magazine Nature Communications.

Dr. Taro Yasoma of Mai University, a doctor and author of the first manuscript, said that the total diabetic fibrosis is a major cause of kidney failure all over the world, yet the main engines remained a mystery, and no treatments can stop the process.

Yasuma said: “Many people with long -term diabetes develop kidney fibrosis, and as soon as it is presented, there are limited options that exceed dialysis or kidney transplantation. Current treatments are mainly focused on controlling blood sugar and blood pressure, but there is no treatment that stops or reflects the scar or fiber.”

The researchers began to examine blood and urine for patients with diabetes. They found that patients have a much more corecene than their healthy counterparts, and that the amount of korisin in the blood is associated with the extent of kidney damage.

When seeing the same results in mice with kidney fibrosis, researchers follow what Corcycin was doing in the kidneys of mice. They found that Corresin accelerates aging in kidney cells, which expels a series of reaction from inflammation to the cell death to the accumulation of scar tissue, which ultimately leads to the loss of kidney function and lining fibrosis.

But how did Corisin get from the intestine to the kidneys? Cann and Gabzza groups with U. of II Chemical and Biominering Profesor Diwakar Shukla to produce computer simulation and laboratory experiences to follow the Corisin trip from the intestine to the bloodstream. They found that corisin can be attached to the albumin, one of the most common proteins in the blood, and riding it through the bloodstream. When you reach the kidneys, Corcycin is separated from the albumin to attack the sensitive structures that nominate blood and urine.

To emphasize that Corresin was the main perpetrator behind kidney damage, researchers gave antibodies against Corcin. They have seen a significant decrease in kidney damage.

“When we treated the mice with an anti -koreceen body, the aging of the kidney cells and reduced kidney scars significantly,” said Gabaza, who is also an assistant animal science professor in Illinois. “Although no such antibody is currently adopting for use in humans, the results we have reached indicate that it can be developed into a new treatment.”

After that, researchers plan to test anti -animal treatments in more advanced animal models, such as pigs, to explore how to adapt them to safe use in humans. U. of I. and MIE University has a disclosure of a joint invention on antibodies to the anti -Corresin.

“Our work indicates that preventing Corresin, either with antibodies or other targeted treatments, can slow or prevent kidney scar in diabetes and thus enhance the quality of life for patients.”

This study was supported by the Science and Technology Agency in Japan, the Japanese Association for the Employment of Science, and the Takeda Foundation,

The Japan Association for Diabetes Education and Care, and the Innovation Research Scholarship in Japan Eli Lily, Dawa Security Foundation, Charles Foundation and Margaret Levin. He was also a professor of microbiology and food science and a member of the East Asian Studies Center in Illinois.