TY - JOUR
T1 - Lipocalin-2
T2 - A novel link between the injured kidney and the bone
AU - Courbon, Guillaume
AU - David, Valentin
N1 - Funding Information:
G.C. has nothing to disclose. V.D. received research funding from Akebia and from Vifor Pharma and consulting honoraria from Keryx Biopharmaceuticals, Vifor Pharma, Luitpold and Amgen outside of submitted work.
Funding Information:
This study was supported by grants from National Institute of Health to V.D. (R01DK102815, R01DK114158).
Publisher Copyright:
© 2022 Lippincott Williams and Wilkins. All rights reserved.
PY - 2022/7/1
Y1 - 2022/7/1
N2 - Purpose of reviewFibroblast growth factor 23 (FGF23) excess is associated with left ventricular hypertrophy (LVH) and early mortality in patients with chronic kidney disease (CKD) and in animal models. Elevated Lipocalin-2 (LCN2), produced by the injured kidneys, contributes to CKD progression and might aggravate cardiovascular outcomes. The current review aims to highlight the role of LCN2 in CKD, particularly its interactions with FGF23.Recent findingsInflammation, disordered iron homeostasis and altered metabolic activity are common complications of CKD, and are associated with elevated levels of kidney-produced LCN2 and bone-secreted FGF23. A recent study shows that elevated LCN2 increases FGF23 production, and contributes to cardiac injury in patients and animals with CKD, whereas LCN2 reduction in mice with CKD reduces FGF23, improves cardiovascular outcomes and prolongs lifespan.SummaryIn this manuscript, we discuss the potential pathophysiological functions of LCN2 as a major kidney-bone crosstalk molecule, linking the progressive decline in kidney function to excessive bone FGF23 production. We also review associations of LCN2 with kidney, cardiovascular and bone and mineral alterations. We conclude that the presented data support the design of novel therapeutic approaches to improve outcomes in CKD.
AB - Purpose of reviewFibroblast growth factor 23 (FGF23) excess is associated with left ventricular hypertrophy (LVH) and early mortality in patients with chronic kidney disease (CKD) and in animal models. Elevated Lipocalin-2 (LCN2), produced by the injured kidneys, contributes to CKD progression and might aggravate cardiovascular outcomes. The current review aims to highlight the role of LCN2 in CKD, particularly its interactions with FGF23.Recent findingsInflammation, disordered iron homeostasis and altered metabolic activity are common complications of CKD, and are associated with elevated levels of kidney-produced LCN2 and bone-secreted FGF23. A recent study shows that elevated LCN2 increases FGF23 production, and contributes to cardiac injury in patients and animals with CKD, whereas LCN2 reduction in mice with CKD reduces FGF23, improves cardiovascular outcomes and prolongs lifespan.SummaryIn this manuscript, we discuss the potential pathophysiological functions of LCN2 as a major kidney-bone crosstalk molecule, linking the progressive decline in kidney function to excessive bone FGF23 production. We also review associations of LCN2 with kidney, cardiovascular and bone and mineral alterations. We conclude that the presented data support the design of novel therapeutic approaches to improve outcomes in CKD.
KW - fibroblast growth factor 23
KW - inflammation
KW - kidney injury
KW - left ventricular hypertrophy
KW - neutrophil gelatinase-associated lipocalin
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U2 - 10.1097/MNH.0000000000000804
DO - 10.1097/MNH.0000000000000804
M3 - Review article
C2 - 35727169
AN - SCOPUS:85132299621
SN - 1062-4821
VL - 31
SP - 312
EP - 319
JO - Current opinion in nephrology and hypertension
JF - Current opinion in nephrology and hypertension
IS - 4
ER -