Loss of salt and body fluids can stimulate kidney regeneration and repair in mice, according to a study led by stem cell scientist Janos Peti-Peterdi of the Keck School of Medicine at the University of Southern California.
This regenerative response relies on a small population of kidney cells in a region known as the macula dense (MD), which detects salt and exerts control over filtration, hormone secretion and other key functions of this vital organ, according to the published study. in The Journal of Clinical Research.
Currently, there is no cure for this silent disease. When kidney disease is diagnosed, the kidneys are irreversibly damaged and ultimately need replacement therapies, such as dialysis or transplant.
To address this growing epidemic, Peti-Peterdi, first author Georgina Gyarmati, and her colleagues took a very untraditional approach.
Instead of studying how diseased kidneys fail to regenerate, scientists focused on how healthy kidneys originally evolved.
The team fed laboratory mice a very low-salt diet, along with a commonly prescribed medication called an ACE inhibitor that further reduced salt and fluid levels.
The mice followed this regimen for up to two weeks, as extremely low-salt diets can trigger serious health problems if continued long term.
In the MD region, the scientists observed regenerative activity, which they were able to block by administering drugs that interfere with the signals sent by the MD.
When the scientists further analyzed the mouse MD cells, they identified both genetic and structural features that were strikingly similar to those of nerve cells.
In mouse MD cells, the scientists also identified specific signals from certain genes, which could be improved by a low-salt diet to regenerate kidney structure and function.
"We strongly believe in the importance of this new way of thinking about kidney repair and regeneration," Peti-Peterdi said. "And we are fully convinced that, hopefully, this will soon end in a new and very powerful therapeutic approach."
This regenerative response relies on a small population of kidney cells in a region known as the macula dense (MD), which detects salt and exerts control over filtration, hormone secretion and other key functions of this vital organ, according to the published study. in The Journal of Clinical Research.
Currently, there is no cure for this silent disease. When kidney disease is diagnosed, the kidneys are irreversibly damaged and ultimately need replacement therapies, such as dialysis or transplant.
To address this growing epidemic, Peti-Peterdi, first author Georgina Gyarmati, and her colleagues took a very untraditional approach.
Instead of studying how diseased kidneys fail to regenerate, scientists focused on how healthy kidneys originally evolved.
The team fed laboratory mice a very low-salt diet, along with a commonly prescribed medication called an ACE inhibitor that further reduced salt and fluid levels.
The mice followed this regimen for up to two weeks, as extremely low-salt diets can trigger serious health problems if continued long term.
In the MD region, the scientists observed regenerative activity, which they were able to block by administering drugs that interfere with the signals sent by the MD.
When the scientists further analyzed the mouse MD cells, they identified both genetic and structural features that were strikingly similar to those of nerve cells.
In mouse MD cells, the scientists also identified specific signals from certain genes, which could be improved by a low-salt diet to regenerate kidney structure and function.
"We strongly believe in the importance of this new way of thinking about kidney repair and regeneration," Peti-Peterdi said. "And we are fully convinced that, hopefully, this will soon end in a new and very powerful therapeutic approach."
