TY - JOUR
T1 - Novel tubular–glomerular interplay in diabetic kidney disease mediated by sirtuin 1, nicotinamide mononucleotide, and nicotinamide adenine dinucleotide Oshima Award Address 2017
AU - Hasegawa, Kazuhiro
N1 - Funding Information:
I would like to thank the Japanese Society of Nephrology for this award. I owe much of my personal success to collaborations with my colleagues, mostly postgraduate students, and to the spectacular mentorship by Drs. Shu Wakino and Hiroshi Itoh in Keio University School of Medicine.
Funding Information:
I would like to thank the Japanese Society of Nephrology for this award. I owe much of my personal success to collaborations with my colleagues, mostly postgraduate students, and to the spectacular mentorship by Drs. Shu Wakino and Hiroshi Itoh in Keio University School of Medicine.
Publisher Copyright:
© 2019, The Author(s).
PY - 2019/8/1
Y1 - 2019/8/1
N2 - Tubules interact with glomeruli, which are composed of podocytes, parietal epithelial cells, mesangial cells, and glomerular endothelial cells. Glomerular–tubular balance and tubuloglomerular feedback are the two components of the tubular–glomerular interplay, which has been demonstrated to play roles in physiological renal function and in diabetic kidney disease (DKD), in which proteins leaking from glomeruli arrive at tubular regions, leading to further tubular injury caused by the accumulation of proteinuria-inducing reactive oxygens species and various cytokines. In the current review, we present our recent work identifying a novel tubular–glomerular interplay in DKD mediated by sirtuin 1 and nicotinamide mononucleotide.
AB - Tubules interact with glomeruli, which are composed of podocytes, parietal epithelial cells, mesangial cells, and glomerular endothelial cells. Glomerular–tubular balance and tubuloglomerular feedback are the two components of the tubular–glomerular interplay, which has been demonstrated to play roles in physiological renal function and in diabetic kidney disease (DKD), in which proteins leaking from glomeruli arrive at tubular regions, leading to further tubular injury caused by the accumulation of proteinuria-inducing reactive oxygens species and various cytokines. In the current review, we present our recent work identifying a novel tubular–glomerular interplay in DKD mediated by sirtuin 1 and nicotinamide mononucleotide.
KW - Diabetic kidney disease
KW - Nicotinamide mononucleotide
KW - Sirtuin 1
KW - Tubuloglomerular feedback
UR - http://www.scopus.com/inward/record.url?scp=85062793966&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85062793966&partnerID=8YFLogxK
U2 - 10.1007/s10157-019-01719-4
DO - 10.1007/s10157-019-01719-4
M3 - Review article
C2 - 30859351
AN - SCOPUS:85062793966
SN - 1342-1751
VL - 23
SP - 987
EP - 994
JO - Clinical and Experimental Nephrology
JF - Clinical and Experimental Nephrology
IS - 8
ER -
