Scientists identify kidney fibrosis pathway

An estimated 10 percent of the world’s population has chronic kidney disease. Photo by Debbie Hill/UPI | Jan. 29 (UPI) — Scientists have pinpointed a cause of chronic kidney disease, a discovery that could soon lead to future treatment for the condition.

Researchers have identified a connection between two keys to the formation of kidney fibrosis progression: a special compartment and a protein, according to research published this month in Science Translational Medicine.

Kidney fibrosis occurs when connective tissue attached to the organ scars and can develop into chronic kidney disease.

"As a disease mechanism, fibrosis may account for more deaths than any other," said corresponding author Joseph Bonventre, who runs Renal Medicine at the Brigham and Women’s Hospital and study author. "Our lab has been studying acute and chronic kidney injury and fibrosis for many years. We’re now focused on the transition from acute to chronic kidney disease and what leads to fibrosis in the kidneys."

The researchers first learned that the target of rapamycin-autophagy spatial coupling compartment, or TASCC, raised the number of secretions that help form kidney fibrosis.

When the team noticed that the protein cyclin G1, or CG1, actually helped create TASCC, they were able to block the formation. Preventing the TASCC’s formation ultimately helped reduce the severity of the progression of kidney fibrosis in lab mice during a preclinical trial.

This new development matters because chronic kidney disease is a massive problem globally. An estimated 10 percent of the world’s population has chronic kidney disease, including 30 million people in the U.S. Chronic kidney disease is also the ninth leading cause of death for Americans, according to the Kidney Fund .

The two main risk factors for developing chronic kidney disease are diabetes and high blood pressure.

"We have identified a mechanism of fibrosis progression involving the induction of CG1-promoted TASCC formation, which facilitates profibrotic factor secretion in cells in the G2-M phase of the cell cycle," the authors wrote. "This pathway may represent a new promising therapeutic target."

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