Abstract
A dipeptidyl peptidase inhibitor, evogliptin, directly prevents nephrin loss and podocyte damage via post-transcriptional regulation
Highlights
BackgroundChronic kidney disease (CKD) affects over 10% of the population worldwide and is an independent risk factor for adverse cardiovascular outcomes [1]
Type 2 diabetes is the most common cause of CKD, and in the United States, >40% of diabetic patients have diabetic nephropathy (DN), which is the main complication of type 2 diabetes and leads to thickening of the glomerular basement membrane, glomerular hypertrophy, mesangial expansion, and overt renal disease [2]
In line with the trend in urinary nephrin excretion, renal nephrin levels in the STZ control group stayed lower at nearly 70% those in the normal control group, and evogliptin and linagliptin alone showed a tendency to restore levels but the difference fell short of statistical significance (Supplementary Figure 1)
Summary
BackgroundChronic kidney disease (CKD) affects over 10% of the population worldwide and is an independent risk factor for adverse cardiovascular outcomes [1]. Type 2 diabetes is the most common cause of CKD, and in the United States, >40% of diabetic patients have diabetic nephropathy (DN), which is the main complication of type 2 diabetes and leads to thickening of the glomerular basement membrane, glomerular hypertrophy, mesangial expansion, and overt renal disease [2]. A 180 kDa, trans-membrane protein in podocytes, was the first molecule identified in the slit between podocyte foot processes and is a major component of the slit diaphragm [5]. In addition to podocyte loss, reduced nephrin levels may lead to development of proteinuria. Loss of podocytes due to podocyte damage leads to impairment of renal filtration function, thereby bringing about proteinuria in glomerular diseases. Dipeptidyl peptidase 4 (DPP4) inhibitors are reported to protect against podocyte damage in preclinical animal models. The direct effects of DPP4 inhibitors on podocytes are not yet fully understood
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
