Chronic kidney disease (CKD) is a public health issue that can be considered pandemic, as it affects 11% of the world’s population and is increasingly common due to an ageing society. CKD is characterised by fibrosis and the permanent infiltration of inflammatory cells, resulting in kidney failure. Emerging research shows microRNAs (miRNAs) can regulate renal fibrosis in CKD, which has resulted in a new treatment target.
- This project represents an innovative approach for treating CKD with miRNA127 (miR127) as a crucial mediator for renal fibrosis.
Problem to Solve
The continuous increase in the prevalence of CKD calls for a lasting solution to slow down the onset and progression of the disease. Several efforts in detecting CKD in its early stages have been successfully implemented in regular clinical practice (for high blood pressure, glucose and albuminuria, among other factors). Nonetheless, in patients with chronic and irreversible disease, prevention is still insufficient. Most current drugs fail due to the severity and frequency of adverse side effects. On top of that, researchers still lack a comprehensive understanding of renal fibrosis on a molecular level.
The discovery of miR127 as an effective regulator of chronic renal damage makes it an excellent therapeutic target. In a lab model, an overexpression of miR127 reduces renal fibrosis. Most importantly, miR127 can be secreted by the fibrotic microenvironment and can stimulate macrophages, making it a critical mediator of the fibrotic process in the kidneys.
Level of Innovation
The approach of modulating miRNAs has become increasingly important as an alternative strategy to stop the disease from progressing. The fact that miR127 has been designed to act in a tissue-specific manner is a promising opportunity to tackle this global medical issue.