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| http://dx.doi.org/10.1093/ndt/gfz186 | DOI Listing |
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Apolipoprotein-L Functions in Membrane Remodeling.
Cells
December 2024
Laboratory of Molecular Parasitology, Institut de Biologie et de Médecine Moléculaires (IBMM), Université Libre de Bruxelles, 6041 Gosselies, Belgium.
The mammalian Apolipoprotein-L families (APOLs) contain several isoforms of membrane-interacting proteins, some of which are involved in the control of membrane dynamics (traffic, fission and fusion). Specifically, human APOL1 and APOL3 appear to control membrane remodeling linked to pathogen infection. Through its association with Non-Muscular Myosin-2A (NM2A), APOL1 controls Golgi-derived trafficking of vesicles carrying the lipid scramblase Autophagy-9A (ATG9A).
View Article and Find Full Text PDFSmall molecule APOL1 inhibitors as a precision medicine approach for APOL1-mediated kidney disease.
Nat Commun
January 2025
Vertex Pharmaceuticals Incorporated, Boston, MA, USA.
Chronic kidney disease affects ~10% of people worldwide and there are no disease modifying therapeutics that address the underlying cause of any form of kidney disease. Genome wide association studies have identified the G1 and G2 variants in the apolipoprotein L1 (APOL1) gene as major contributors to a subtype of proteinuric kidney disease now referred to as APOL1-mediated kidney disease (AMKD). We hypothesized that inhibition of APOL1 could have therapeutic potential for this genetically-defined form of kidney disease.
View Article and Find Full Text PDFSteroid-Resistant Nephrotic Syndrome Is Associated With a Unique Genetic Profile in a Highly Admixed Pediatric Population.
Kidney Int Rep
December 2024
Division of Molecular Medicine, University of São Paulo School of Medicine, São Paulo, Brazil.
Introduction: The profile of genetic and nongenetic factors associated with progression to kidney failure (KF) in steroid-resistant nephrotic syndrome (SRNS) is largely unknown in admixed populations.
Methods: A total of 101 pediatric patients with primary SRNS were genetically assessed targeting Mendelian causes and status with a 62-NS-gene panel or whole exome sequencing, as well as genetic ancestry. Variant pathogenicity was evaluated using the American College Medical of Genetics and Genomics (ACMG) criteria.
ApoL1 risk allele accelerates high-fat diet-induced atherosclerosis in LDLR hamsters.
Genes Dis
March 2025
Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing 100191, China.
The APOL1 p.N264K variant is co-inherited with the G2 kidney disease risk variant through a proximity recombination event.
G3 (Bethesda)
December 2024
Harvard Medical School, Boston, MA, 02215, USA.
Black Americans are three to four times more likely to develop nondiabetic kidney disease than other populations. Exclusively found in people of recent African (AFR) ancestry, risk variants in Apolipoprotein L1 (APOL1) termed G1 and G2 contribute significantly to this increased susceptibility. Our group and others showed that a missense variant in APOL1, rs73885316 (p.
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