TY - JOUR
T1 - Apolipoprotein L1 nephropathies
T2 - 2017 in review
AU - Kopp, Jeffrey B.
AU - Roshanravan, Hila
AU - Okamoto, Koji
N1 - Funding Information:
The authors were supported by the Intramural Research Program, NIDDK, NIH.
Publisher Copyright:
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
PY - 2018/5/1
Y1 - 2018/5/1
N2 - Purpose of review To review publications relating to apolipoprotein L1 (APOL1) renal risk variants published 2017. Recent findings The study of APOL1 variants continues to be highly active; 24 articles published in 2017 were selected to highlight. These include clinical studies of kidney disease, kidney transplantation, hypertension, cardiovascular disease, and genetic diversity. Laboratory studies included APOL1 association with vesicle-associated membrane soluble N-ethylmaleimide-sensitive factor activating protein receptor protein and with soluble urokinase-type plasminogen activator receptor, mitochondrial dysfunction, endolysosomal dysfunction, and inflammasome activation. Summary Our understanding of the role of APOL1 genetic variants and the mechanisms for renal toxicity continues to deepen. It is not yet clear which pathways are most relevant to human disease, and so, the most relevant drug targets remain to be defined.
AB - Purpose of review To review publications relating to apolipoprotein L1 (APOL1) renal risk variants published 2017. Recent findings The study of APOL1 variants continues to be highly active; 24 articles published in 2017 were selected to highlight. These include clinical studies of kidney disease, kidney transplantation, hypertension, cardiovascular disease, and genetic diversity. Laboratory studies included APOL1 association with vesicle-associated membrane soluble N-ethylmaleimide-sensitive factor activating protein receptor protein and with soluble urokinase-type plasminogen activator receptor, mitochondrial dysfunction, endolysosomal dysfunction, and inflammasome activation. Summary Our understanding of the role of APOL1 genetic variants and the mechanisms for renal toxicity continues to deepen. It is not yet clear which pathways are most relevant to human disease, and so, the most relevant drug targets remain to be defined.
KW - arterionephrosclerosis
KW - endolysosomal trafficking
KW - inflammasome
KW - kidney transplantation
KW - mitochondria
KW - soluble urokinase-type plasminogen activator receptor
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U2 - 10.1097/MNH.0000000000000399
DO - 10.1097/MNH.0000000000000399
M3 - Review article
C2 - 29389775
AN - SCOPUS:85045155493
SN - 1062-4821
VL - 27
SP - 153
EP - 158
JO - Current Opinion in Nephrology and Hypertension
JF - Current Opinion in Nephrology and Hypertension
IS - 3
ER -