ArticlePloS one2019
APOL1 renal risk variants promote cholesterol accumulation in tissues and cultured macrophages from APOL1 transgenic mice.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 67 citations in OpenAlex.
- Therapeutic Regulation of Macrophage Polarization for Diabetic Kidney Disease by Targeted Metabolic Reprogramming.Current medical science · 2026Review
- Apolipoproteins L involvement in immunity.Journal of human immunity · 2026Review
- APOL1 G1 and G2 risk alleles modulate severity of diet-induced obesity in a transgenic mouse model.bioRxiv : the preprint server for biology · 2025Article
- APOL1-mediated kidney disease: a narrative review of the lessons learnt from the past 15 years.BMC nephrology · 2025Review
- APOL1 risk variants induce metabolic reprogramming of podocytes in patient-derived kidney organoids.Stem cell reports · 2025Article
- Sodium-glucose co-transporter inhibitors for APOL1 kidney disease: A call for studies.International urology and nephrology · 2025Review
- G1 and G2 ApolipoproteinL1 modulate macrophage inflammation and lipid accumulation through the polyamine pathway.bioRxiv : the preprint server for biology · 2025Article
- Apolipoprotein-L1 G1 variant contributes to hydrocephalus but not to atherosclerosis in apolipoprotein-E knock-out mice.Clinical science (London, England : 1979) · 2025Article
- APOL4-mediated intracellular cholesterol trafficking is essential for glioblastoma cell growth.BMC cancer · 2025Article
- High-Density Lipoprotein Lipid and Protein Cargo and Cholesterol Efflux Capacity Before and After Bariatric Surgery.Arteriosclerosis, thrombosis, and vascular biology · 2025Observational
- Review
- The Kidney in Obesity: Current Evidence, Perspectives and Controversies.Current obesity reports · 2024Review
- Pathogenesis of HIV-associated nephropathy in children and adolescents: taking a hard look 40 years later in the era of gene-environment interactions.American journal of physiology. Renal physiology · 2024Review
- Review
- APOL1 polymorphisms are not influencing acute coronary syndrome risk in Czech males.Molecular genetics & genomic medicine · 2024Article
- Cardiometabolic comorbidities and complications of obesity and chronic kidney disease (CKD).Journal of clinical & translational endocrinology · 2024Review
- Tubular deficiency of ABCA1 augments cholesterol- and NaAmerican journal of physiology. Renal physiology · 2024Article
- HIF-2α/LINC02609/APOL1-mediated lipid storage promotes endoplasmic reticulum homeostasis and regulates tumor progression in clear-cell renal cell carcinoma.Journal of experimental & clinical cancer research : CR · 2024Article
- APOL1-mediated monovalent cation transport contributes to APOL1-mediated podocytopathy in kidney disease.The Journal of clinical investigation · 2024Article
- Unveiling the pathogenesis and therapeutic approaches for diabetic nephropathy: insights from panvascular diseases.Frontiers in endocrinology · 2024Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Apolipoprotein L1 (APOL1) genetic variants G1 and G2, compared to the common allele G0, are major risk factors for non-diabetic kidney disease in African descent populations. APOL1 is a minor protein component of HDL, as well as being expressed in podocytes and vascular cells. Reverse cholesterol transport involves the transport of cholesterol to HDL by cellular ATP-binding cassette; ABCA1 and ABCG1 with subsequent delivery from peripheral tissues to the liver. With impaired reverse cholesterol transport, lipid accumulation occurs and macrophages morphologically transform into foam cells, releasing inflammatory factors. We asked whether the APOL1 risk variants alter peripheral cholesterol metabolism and specifically affect macrophage cholesterol efflux. Tissues and bone marrow (BM)-derived monocytes were isolated from wild-type mice (WT) and from BAC/APOL1 transgenic (APOL1-G0, APOL1-G1, and APOL1-G2) mice, which carry a bacterial artificial chromosome that contains the human APOL1 genomic region. Monocytes were differentiated into macrophages using M-CSF, and then polarized into M1 and M2 macrophages. Cholesterol content, cholesterol efflux, and ABCA1 and ABCG1 mRNA expression were measured. Kidney, spleen, and bone marrow-derived macrophages from APOL1-G1 and -G2 mice showed increased cholesterol accumulation and decreased ABCA1 and ABCG1 mRNA levels. BM-derived macrophages from APOL1-G1 and -G2 mice showed significantly reduced cholesterol efflux compared to WT or APOL1-G0 macrophages. Taken together, the evidence suggests that APOL1-G1 and -G2 risk variants impaired reverse cholesterol transport through decreased expression of cholesterol efflux transporters suggesting a possible mechanism to promote macrophage foam cell formation, driving inflammation in the glomerulus and renal interstitium.
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Registered trials
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