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Research Into Key Protein Could Lead to Target to Halt CKD


Experiments with the protein Cx43 show that it could be a "druggable target" to prevent renal decline.

A new study from the United Kingdom has shed light on an emerging area of research in chronic kidney disease (CKD), involving proteins that govern cell communication—and a particular one that plays a role in setting off kidney failure.

Led by Claire Hills, PhD, associate professor in the School of Life Sciences, University of Lincoln, the study appearing in Cell Communication and Signaling involves proteins called connexins. According to a statement from the university, these proteins typically regulate communication between healthy kidney cells.

“If these connexins fail, signaling molecules spill into the organ and set off a chain of events that can ultimately lead to kidney failure. One connexin—called Cx43—actually makes the whole situation worse, so our new research set out to effectively block Cx43," Hills said in a statement "By providing insight into the initiating trigger for early injury in chronic kidney disease, we expose the tantalizing prospect that by altering the tone of conversation between cells we could prevent kidney damage and slow disease progression."

CKD is increasing as the rates of diabetes and obesity rise and the population ages; once a patient is in kidney failure, treatment with dialysis is among the most expensive and debilitating treatments in health care.

To explore the role of Cx43 in declining kidney function, the investigators observed its role in the release of adenosine triphosphate (ATP), causing early tubular damage. They then used another protein called Peptide 5, to block this effect, and even restore some cell function.

“Since Cx43 is highly expressed in nephropathy, it represents a novel target for intervention of tubulointerstitial fibrosis in CKD,” the investigators concluded.

“This work shows how we used Peptide 5 to block small holes that appear in the outer layer of kidney cells in people with diabetes,” Lincoln University’s Paul Squires, PhD, BSc, added. “By blocking these holes and reducing the release of 'bad signals' from the kidneys, we can control how cells talk to each other and decrease the amount of inflammation that can normally be seen in chronic kidney disease."

The findings represent discovery of a “druggable target for patients with CKD,” Squires said.


Price GW, Chadjichristos CE, Kavvadas P, et al. Blocking Connexin-43 mediated hemichannel activity protects against early tubular injury in experimental chronic kidney disease. Cell Commun Signal. 2020;18(1):79. doi: 10.1186/s12964-020-00558-1

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