ArticleAmerican journal of physiology. Renal physiology2018
Loss of biliverdin reductase-A promotes lipid accumulation and lipotoxicity in mouse proximal tubule cells.
Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 71 citations in OpenAlex.
- Citrate-Dependent Activation of Acetyl CoA Carboxylase Promotes Renal Lipid Accumulation in a Rat Model of Chronic Kidney Disease.Acta physiologica (Oxford, England) · 2026Article
- Loss of the CoA-degrading enzyme NUDT19 exacerbates albuminuria and disrupts renal lipid homeostasis in high fat diet-fed mice.Scientific reports · 2026Article
- Ectopic lipid deposition in kidney diseases: mechanisms in specific cell types and therapeutic strategies.Frontiers in endocrinology · 2026Review
- The Inflammation Effect in the Association Between Bilirubin and Chronic Kidney Disease in Patients with Type 2 Diabetes: A Retrospective Cohort Study.Journal of inflammation research · 2026Article
- Perinephric fat volume and its negative correlation with the eGFR according to a population health screening: a cross-sectional study.Renal failure · 2025Article
- Bilirubin Hepatic and Intestinal Transport and Catabolism: Physiology, Pathophysiology, and Benefits.Antioxidants (Basel, Switzerland) · 2025Review
- Bilirubin bioconversion to urobilin in the gut-liver-kidney axis: A biomarker for insulin resistance in the Cardiovascular-Kidney-Metabolic (CKM) Syndrome.Metabolism: clinical and experimental · 2025Review
- Assessing Association Between Circulating Bilirubin Levels and the Risk of Frailty: An Observational and Mendelian Randomization Study.Journal of cachexia, sarcopenia and muscle · 2025Observational
- Heme oxygenase, biliverdin reductase, and bilirubin pathways regulate oxidative stress and insulin resistance: a focus on diabetes and therapeutics.Clinical science (London, England : 1979) · 2025Review
- Urobilin Derived from Bilirubin Bioconversion Binds Albumin and May Interfere with Bilirubin Interacting with Albumin: Implications for Disease Pathology.Biomedicines · 2025Article
- Relationship between nontraditional lipid parameters and the risk of type 2 diabetes in individuals recovered from dyslipidemia: a cohort study.Frontiers in endocrinology · 2025Article
- Molecular Insight into Obesity-Associated Nephropathy: Clinical Implications and Possible Strategies for its Management.Current drug targets · 2025Review
- Association between cumulative average triglyceride glucose-body mass index and the risk of CKD onset.Frontiers in endocrinology · 2025Article
- Advances of Iron and Ferroptosis in Diabetic Kidney Disease.Kidney international reports · 2024Review
- Species-specific histological characterizations of renal tubules and collecting ducts in the kidneys of cats and dogs.PloS one · 2024Article
- Article
- Childhood Obesity: Insight into Kidney Involvement.International journal of molecular sciences · 2023Review
- Targeting Renal Proximal Tubule Cells in Obesity-Related Glomerulopathy.Pharmaceuticals (Basel, Switzerland) · 2023Review
- High-fat diet causes mitochondrial damage and downregulation of mitofusin-2 and optic atrophy-1 in multiple organs.Journal of clinical biochemistry and nutrition · 2023Article
- Severe Hypertriglyceridaemia and Chylomicronaemia Syndrome-Causes, Clinical Presentation, and Therapeutic Options.Metabolites · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Obesity and increased lipid availability have been implicated in the development and progression of chronic kidney disease. One of the major sites of renal lipid accumulation is in the proximal tubule cells of the kidney, suggesting that these cells may be susceptible to lipotoxicity. We previously demonstrated that loss of hepatic biliverdin reductase A (BVRA) causes fat accumulation in livers of mice on a high-fat diet. To determine the role of BVRA in mouse proximal tubule cells, we generated a CRISPR targeting BVRA for a knockout in mouse proximal tubule cells (BVRA KO). The BVRA KO cells had significantly less metabolic potential and mitochondrial respiration, which was exacerbated by treatment with palmitic acid, a saturated fatty acid. The BVRA KO cells also showed increased intracellular triglycerides which were associated with higher fatty acid uptake gene cluster of differentiation 36 as well as increased de novo lipogenesis as measured by higher neutral lipids. Additionally, neutrophil gelatinase-associated lipocalin 1 expression, annexin-V FITC staining, and lactate dehydrogenase assays all demonstrated that BVRA KO cells are more sensitive to palmitic acid-induced lipotoxicity than wild-type cells. Phosphorylation of BAD which plays a role in cell survival pathways, was significantly reduced in palmitic acid-treated BVRA KO cells. These data demonstrate the protective role of BVRA in proximal tubule cells against saturated fatty acid-induced lipotoxicity and suggest that activating BVRA could provide a benefit in protecting from obesity-induced kidney injury.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.