Therapeutics for APOL1 nephropathies: putting out the fire in the podocyte
APOL1 nephropathies comprise a range of clinical and pathologic syndromes, which can be summarized as focal segmental glomerulosclerosis, in various guises, and arterionephrosclerosis, otherwise known as hypertensive kidney diseases. Current therapies for these conditions may achieve therapeutic tar...
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Published in | Nephrology, dialysis, transplantation Vol. 32; no. suppl_1; pp. i65 - i70 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
England
Oxford University Press
01.01.2017
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Abstract | APOL1 nephropathies comprise a range of clinical and pathologic syndromes, which can be summarized as focal segmental glomerulosclerosis, in various guises, and arterionephrosclerosis, otherwise known as hypertensive kidney diseases. Current therapies for these conditions may achieve therapeutic targets, reduction in proteinuria and control of blood pressure, respectively, but often fail to halt the progressive decline in kidney function. It appears that current therapies fail to address certain underlying critical pathologic processes that are driven, particularly in podocytes and microvascular cells, by the APOL1 renal risk genetic variants. Mechanisms hypothesized to be responsible for APOL1 variant-associated cell injury can be summarized in five domains: increased APOL1 gene expression, activation of inflammasomes, activation of protein kinase R, electrolyte flux across plasma or intracellular membranes, and altered endolysosomal trafficking associated with endoplasmic reticulum stress. We briefly review the available evidence for these five mechanisms and suggest possible novel therapeutic approaches. |
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AbstractList | APOL1 nephropathies comprise a range of clinical and pathologic syndromes, which can be summarized as focal segmental glomerulosclerosis, in various guises, and arterionephrosclerosis, otherwise known as hypertensive kidney diseases. Current therapies for these conditions may achieve therapeutic targets, reduction in proteinuria and control of blood pressure, respectively, but often fail to halt the progressive decline in kidney function. It appears that current therapies fail to address certain underlying critical pathologic processes that are driven, particularly in podocytes and microvascular cells, by the
APOL1
renal risk genetic variants. Mechanisms hypothesized to be responsible for APOL1 variant-associated cell injury can be summarized in five domains: increased
APOL1
gene expression, activation of inflammasomes, activation of protein kinase R, electrolyte flux across plasma or intracellular membranes, and altered endolysosomal trafficking associated with endoplasmic reticulum stress. We briefly review the available evidence for these five mechanisms and suggest possible novel therapeutic approaches. APOL1 nephropathies comprise a range of clinical and pathologic syndromes, which can be summarized as focal segmental glomerulosclerosis, in various guises, and arterionephrosclerosis, otherwise known as hypertensive kidney diseases. Current therapies for these conditions may achieve therapeutic targets, reduction in proteinuria and control of blood pressure, respectively, but often fail to halt the progressive decline in kidney function. It appears that current therapies fail to address certain underlying critical pathologic processes that are driven, particularly in podocytes and microvascular cells, by the APOL1 renal risk genetic variants. Mechanisms hypothesized to be responsible for APOL1 variant-associated cell injury can be summarized in five domains: increased APOL1 gene expression, activation of inflammasomes, activation of protein kinase R, electrolyte flux across plasma or intracellular membranes, and altered endolysosomal trafficking associated with endoplasmic reticulum stress. We briefly review the available evidence for these five mechanisms and suggest possible novel therapeutic approaches. |
Author | Heymann, Jurgen Kopp, Jeffrey B Susztak, Katalin Winkler, Cheryl A Hoek, Maarten |
AuthorAffiliation | 1 Kidney Disease Section, NIDDK, NIH, Bethesda, MD, USA 3 Merck Research Laboratories, Merck and Co., Kenilworth, NJ, USA 4 Renal, Electrolyte, and Hypertension Division, Department of Medicine, Perelman School of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA 2 Molecular Genetic Epidemiology Section, Basic Research Laboratory, Basic Science Program; Leidos Biomedical Research, Frederick National Laboratory, NCI, NIH, Frederick, MD, USA |
AuthorAffiliation_xml | – name: 1 Kidney Disease Section, NIDDK, NIH, Bethesda, MD, USA – name: 2 Molecular Genetic Epidemiology Section, Basic Research Laboratory, Basic Science Program; Leidos Biomedical Research, Frederick National Laboratory, NCI, NIH, Frederick, MD, USA – name: 3 Merck Research Laboratories, Merck and Co., Kenilworth, NJ, USA – name: 4 Renal, Electrolyte, and Hypertension Division, Department of Medicine, Perelman School of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA |
Author_xml | – sequence: 1 givenname: Jurgen surname: Heymann fullname: Heymann, Jurgen organization: Kidney Disease Section, NIDDK, NIH, Bethesda, MD, USA – sequence: 2 givenname: Cheryl A surname: Winkler fullname: Winkler, Cheryl A organization: Molecular Genetic Epidemiology Section, Basic Research Laboratory, Basic Science Program; Leidos Biomedical Research, Frederick National Laboratory, NCI, NIH, Frederick, MD, USA – sequence: 3 givenname: Maarten surname: Hoek fullname: Hoek, Maarten organization: Merck Research Laboratories, Merck and Co., Kenilworth, NJ, USA – sequence: 4 givenname: Katalin surname: Susztak fullname: Susztak, Katalin organization: Renal, Electrolyte and Hypertension Division, Department of Medicine, Perelman School of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA – sequence: 5 givenname: Jeffrey B surname: Kopp fullname: Kopp, Jeffrey B organization: Kidney Disease Section, NIDDK, NIH, Bethesda, MD, USA |
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Copyright | Published by Oxford University Press on behalf of ERA-EDTA 2017. This work is written by US Government employees and is in the public domain in the United States. Published by Oxford University Press on behalf of ERA-EDTA 2017. This work is written by US Government employees and is in the public domain in the United States. 2017 |
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Keywords | chronic kidney disease glomerulosclerosis focal segmental glomerulosclerosis inflammation podocytes |
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Snippet | APOL1 nephropathies comprise a range of clinical and pathologic syndromes, which can be summarized as focal segmental glomerulosclerosis, in various guises,... |
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SubjectTerms | Apolipoprotein L1 Apolipoproteins - antagonists & inhibitors CLINICAL SCIENCE REVIEWS Glomerulosclerosis, Focal Segmental - drug therapy Glomerulosclerosis, Focal Segmental - metabolism Glomerulosclerosis, Focal Segmental - pathology Humans Hypertension, Renal - drug therapy Hypertension, Renal - metabolism Hypertension, Renal - pathology Lipoproteins, HDL - antagonists & inhibitors Nephritis - drug therapy Nephritis - metabolism Nephritis - pathology |
Title | Therapeutics for APOL1 nephropathies: putting out the fire in the podocyte |
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