Researchers found high levels of corisin a small peptide produced by Staphylococcus bacteria in the gut in the blood of patients with diabetic kidney fibrosis and used computer models along with tissue and mouse experiments to trace how it reaches the kidneys triggers damage and could potentially be countered with antibody treatment. Our previous studies showed corisin can harm cells and worsen scarring in other organs so we suspected it might drive kidney fibrosis said Isaac Cann Illinois animal sciences professor who led the study with Mie University’s Dr. Esteban Gabazza. These findings suggest corisin is a hidden culprit behind progressive kidney damage in diabetes and blocking it could offer a new way to protect kidney health.

Diabetic kidney fibrosis a leading cause of kidney failure worldwide has long lacked effective treatments, explained Dr. Taro Yasuma of Mie University, the study’s first author. Many people with longstanding diabetes eventually develop kidney fibrosis, and once it progresses options are limited to dialysis or transplantation. Current therapies mainly manage blood sugar and blood pressure but nothing halts or reverses the scarring process he said. The researchers screened blood and urine from patients with diabetic kidney disease and found significantly higher levels of corisin compared to healthy individuals with blood levels correlating to the severity of kidney damage. Similar results in mice revealed that corisin accelerates aging in kidney cells triggering inflammation cell death and scar tissue buildup, ultimately leading to loss of kidney function and worsening fibrosis.

To understand how corisin travels from the gut to the kidneys Cann and Gabazza’s teams collaborated with University of Illinois chemical and biomolecular engineering professor Diwakar Shukla to combine computer simulations with laboratory experiments. They discovered that corisin binds to albumin a common blood protein which carries it through the bloodstream until it detaches in the kidneys damage the filtering structures. To confirm corisin’s role in kidney injury, the researchers treated mice with antibodies targeting corisin which significantly slowed kidney cell aging and reduced scarring. While no such antibody is yet approved for human use our findings suggest it could potentially be developed into a new therapy said Gabazza adjunct professor of animal sciences at Illinois.

The researchers now plan to test anticorisin treatments in more advanced animal models such as pigs to evaluate their potential for safe human use, with the University of Illinois and Mie University filing a joint invention disclosure on corisin antibodies. Our findings indicate that blocking corisin whether with antibodies or other targeted therapies could slow or prevent kidney scarring in diabetes and improve patients’ quality of life said Cann who is also a professor of microbiology and nutritional sciences and a member of the Center for East Asian and Pacific Studies at Illinois. The study was supported by the Japan Science and Technology Agency the Japan Society for the Promotion of Science, the Takeda Science Foundation the Japan Association for Diabetes Education and Care, the Eli Lilly Japan Innovation Research Grant, the Daiwa Security Foundation, and the Charles and Margaret Levin Family Foundation.

Source: https://news.illinois.edu/kidney-fibrosis-linked-to-molecule-made-by-gut-bacteria/