ArticleThe Journal of pharmacology and experimental therapeutics2019
LCAT Enzyme Replacement Therapy Reduces LpX and Improves Kidney Function in a Mouse Model of Familial LCAT Deficiency.
Article in The Journal of pharmacology and experimental therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.
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Who cites it
18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 27 citations in OpenAlex.
- Role of apolipoprotein C1 in lipoprotein metabolism, atherosclerosis and diabetes: a systematic review.Cardiovascular diabetology · 2022Pooled it
- A systematic review of the natural history and biomarkers of primary lecithin:cholesterol acyltransferase deficiency.Journal of lipid research · 2022Pooled it
- LCAT acts as a molecular switch and regulates rooster sperm motility in vitro.Molecular & cellular proteomics : MCP · 2026Article
- Loss of LCAT function aggravates metabolic-associated steatohepatitis (MASH) in golden Syrian hamster.Clinical science (London, England : 1979) · 2025Article
- Understanding the heterogeneity and dysfunction of HDL in chronic kidney disease: insights from recent reviews.BMC nephrology · 2024Review
- Gliflozins, sucrose and flavonoids are allosteric activators of lecithin-cholesterol acyltransferase.Scientific reports · 2024Article
- Article
- Interaction between Rumen Epithelial miRNAs-Microbiota-Metabolites in Response to Cold-Season Nutritional Stress in Tibetan Sheep.International journal of molecular sciences · 2023Article
- HDL and chronic kidney disease.Atherosclerosis plus · 2023Article
- A rare case of renal involvement in Lecithin-Cholesterol Acyltransferase (LCAT) deficiency: lessons for the clinical nephrologist.Journal of nephrology · 2023Article
- Article
- High Density Lipoproteins: Is There a Comeback as a Therapeutic Target?Handbook of experimental pharmacology · 2022Article
- Lecithin:cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings.Journal of lipid research · 2020Article
- Novel lecithin: cholesterol acyltransferase-based therapeutic approaches.Current opinion in lipidology · 2020Article
- LCAT protects against Lipoprotein-X formation in a murine model of drug-induced intrahepatic cholestasis.Pharmacology research & perspectives · 2020Article
- Sirt6 deficiency aggravates angiotensin II-induced cholesterol accumulation and injury in podocytes.Theranostics · 2020Article
- Plasma lipoprotein-X quantification on filipin-stained gels: monitoring recombinant LCAT treatment ex vivo.Journal of lipid research · 2019Article
- Longitudinal analysis of clinical and laboratory biomarkers in a patient with familial lecithin: cholesterol acyltransferase deficiency (FLD) and accelerated eGFR decline: A case study.Journal of clinical lipidologyArticle
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Familial LCAT deficiency (FLD) is due to mutations in lecithin:cholesterol acyltransferase (LCAT), a plasma enzyme that esterifies cholesterol on lipoproteins. FLD is associated with markedly reduced levels of plasma high-density lipoprotein and cholesteryl ester and the formation of a nephrotoxic lipoprotein called LpX. We used a mouse model in which the LCAT gene is deleted and a truncated version of the SREBP1a gene is expressed in the liver under the control of a protein-rich/carbohydrate-low (PRCL) diet-regulated PEPCK promoter. This mouse was found to form abundant amounts of LpX in the plasma and was used to determine whether treatment with recombinant human LCAT (rhLCAT) could prevent LpX formation and renal injury. After 9 days on the PRCL diet, plasma total and free cholesterol, as well as phospholipids, increased 6.1 ± 0.6-, 9.6 ± 0.9-, and 6.7 ± 0.7-fold, respectively, and liver cholesterol and triglyceride concentrations increased 1.7 ± 0.4- and 2.8 ±0.9-fold, respectively, compared with chow-fed animals. Transmission electron microscopy revealed robust accumulation of lipid droplets in hepatocytes and the appearance of multilamellar LpX particles in liver sinusoids and bile canaliculi. In the kidney, LpX was found in glomerular endothelial cells, podocytes, the glomerular basement membrane, and the mesangium. The urine albumin/creatinine ratio increased 30-fold on the PRCL diet compared with chow-fed controls. Treatment of these mice with intravenous rhLCAT restored the normal lipoprotein profile, eliminated LpX in plasma and kidneys, and markedly decreased proteinuria. The combined results suggest that rhLCAT infusion could be an effective therapy for the prevention of renal disease in patients with FLD.
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