ArticleJournal of the American Society of Nephrology : JASN2016
Deletion of Lkb1 in Renal Tubular Epithelial Cells Leads to CKD by Altering Metabolism.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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73 citing papers in PubMed, 129 citations in OpenAlex.
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- Adipose Mesenchymal Stem Cells Secreted Exosomal miR-26a-5p Ameliorate Renal Fibrosis via Inhibiting Glycolysis and Ferroptosis in Renal Interstitial Fibrosis.Journal of cellular and molecular medicine · 2026Article
- Energy metabolism in the kidney and its role in chronic kidney disease.Clinical and experimental nephrology · 2026Review
- From Single-Cell Clusters to Causality: ITCH Engagement for CKD Uncovered by Integrative Analysis of MR and MAGMA.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Pyruvate Dehydrogenase and Cellular Metabolism in Calcineurin Inhibitor-Induced Kidney Fibrosis.Journal of the American Society of Nephrology : JASN · 2026Article
- Licochalcone A mitigates cisplatin-induced nephrotoxicity by inhibiting ferroptosis and mitochondrial dysfunction via the Nrf2/GPX4 axis.Frontiers in pharmacology · 2026Article
- Dedifferentiated proximal tubular epithelial cells in diabetic kidney disease: pathogenic roles, repair potential, and therapeutic implications.Frontiers in endocrinology · 2026Review
- Co-occurrence of Peutz-Jeghers syndrome and unilateral multicystic dysplastic kidney: a case report.BMC nephrology · 2025Article
- Insights into targeting LKB1 in tumorigenesis.Genes & diseases · 2025Review
- Characterizing Metabolic Shifts in Septic Murine Kidney Tissue Using 2P-FLIM for Early Sepsis Detection.Bioengineering (Basel, Switzerland) · 2025Article
- Metabolism at the crossroads of inflammation and fibrosis in chronic kidney disease.Nature reviews. Nephrology · 2025Review
- Mitochondrial dysfunction and metabolic reprogramming in acute kidney injury: mechanisms, therapeutic advances, and clinical challenges.Frontiers in physiology · 2025Review
- Deficiency of thiosulfate sulfurtransferase mediates the dysfunction of renal tubular mitochondrial fatty acid oxidation in diabetic kidney disease.Cell death and differentiation · 2024Article
- Effect ofAnimal biotechnology · 2024Article
- A brief harvesting-freezing delay significantly alters the kidney metabolome and leads to false positive and negative results.American journal of physiology. Renal physiology · 2024Article
- β-catenin-inhibited Sumoylation modification of LKB1 and fatty acid metabolism is critical in renal fibrosis.Cell death & disease · 2024Article
- The key role of altered tubule cell lipid metabolism in kidney disease development.Kidney international · 2024Review
- LKB1 depletion-mediated epithelial-mesenchymal transition induces fibroblast activation in lung fibrosis.Genes & diseases · 2024Article
- Understanding interleukin 11 as a disease gene and therapeutic target.The Biochemical journal · 2023Review
- SETD2 deficiency accelerates sphingomyelin accumulation and promotes the development of renal cancer.Nature communications · 2023Article
13 more citing papers are in PubMed but not listed here.
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7 authors at 3 institutions in 3 countries.
Funding
Abstract
Renal tubule epithelial cells are high-energy demanding polarized epithelial cells. Liver kinase B1 (LKB1) is a key regulator of polarity, proliferation, and cell metabolism in epithelial cells, but the function of LKB1 in the kidney is unclear. Our unbiased gene expression studies of human control and CKD kidney samples identified lower expression of LKB1 and regulatory proteins in CKD. Mice with distal tubule epithelial-specific Lkb1 deletion (Ksp-Cre/Lkb1(flox/flox)) exhibited progressive kidney disease characterized by flattened dedifferentiated tubule epithelial cells, interstitial matrix accumulation, and dilated cystic-appearing tubules. Expression of epithelial polarity markers β-catenin and E-cadherin was not altered even at later stages. However, expression levels of key regulators of metabolism, AMP-activated protein kinase (Ampk), peroxisome proliferative activated receptor gamma coactivator 1-α (Ppargc1a), and Ppara, were significantly lower than those in controls and correlated with fibrosis development. Loss of Lkb1 in cultured epithelial cells resulted in energy depletion, apoptosis, less fatty acid oxidation and glycolysis, and a profibrotic phenotype. Treatment of Lkb1-deficient cells with an AMP-activated protein kinase (AMPK) agonist (A769662) or a peroxisome proliferative activated receptor alpha agonist (fenofibrate) restored the fatty oxidation defect and reduced apoptosis. In conclusion, we show that loss of LKB1 in renal tubular epithelial cells has an important role in kidney disease development by influencing intracellular metabolism.
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