ArticleKidney international2015
Reduced Krüppel-like factor 2 expression may aggravate the endothelial injury of diabetic nephropathy.
Article in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 63 citations in OpenAlex.
- Endothelial Cell-Pericyte Crosstalk in the Brain Balances Microvascular Stability and Plasticity.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Histone H4K5 deacetylation by enhanced HDAC1 expression drives endothelial inflammation in diabetes through repression of the KLF2-eNOS axis.Human cell · 2026Article
- Deletion of endothelial KLF4 as a model for preeclampsia.bioRxiv : the preprint server for biology · 2026Article
- New potential therapeutic targets of metabolic disorder-associated kidney disease and diabetic kidney disease.Kidney international · 2026Review
- Investigating the mechanisms of lactulose on gut health and uric acid metabolism in geese via transcriptomics.Scientific reports · 2025Article
- Pericyte activation accompanied by peritubular capillaries dysfunction and pericyte-to-myofibroblast transition is associated with renal fibrosis in diabetic nephropathy.Kidney research and clinical practice · 2025Article
- Glyoxalase-1 overexpression attenuates arterial wall stiffening in diabetic mice.Cardiovascular diabetology · 2025Article
- Targeting Krüppel-Like Factor 2 as a Novel Therapy for Glomerular Endothelial Cell Injury in Diabetic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025Article
- Specificity of endothelial cells in endothelial dysfunction of diabetic kidney disease and their crosstalk with neighboring cells: an updated review.Frontiers in endocrinology · 2025Review
- Krüppel-like factor 2 is an endoprotective transcription factor in diabetic kidney disease.American journal of physiology. Cell physiology · 2024Review
- Article
- Crosstalk among podocytes, glomerular endothelial cells and mesangial cells in diabetic kidney disease: an updated review.Cell communication and signaling : CCS · 2024Review
- Plxnd1-mediated mechanosensing of blood flow controls the caliber of the Dorsal Aorta via the transcription factor Klf2.bioRxiv : the preprint server for biology · 2024Article
- Early diabetic kidney disease: Focus on the glycocalyx.World journal of diabetes · 2023Review
- Participation of Krüppel-like Factors in Atherogenesis.Metabolites · 2023Review
- Expanded Hemodialysis ameliorates uremia-induced impairment of vasculoprotective KLF2 and concomitant proinflammatory priming of endothelial cells through an ERK/AP1/cFOS-dependent mechanism.Frontiers in immunology · 2023Article
- Flot2 acts as a novel mediator of podocyte injury in proteinuric kidney disease.International journal of biological sciences · 2023Article
- Cellular crosstalk of glomerular endothelial cells and podocytes in diabetic kidney disease.Journal of cell communication and signaling · 2022Review
- A mitochondrial contribution to anti-inflammatory shear stress signaling in vascular endothelial cells.The Journal of cell biology · 2022Article
- Renoprotective Effect of KLF2 on Glomerular Endothelial Dysfunction in Hypertensive Nephropathy.Cells · 2022Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Krüppel-like factor 2 (KLF2), a shear stress-inducible transcription factor, has endoprotective effects. In streptozotocin-induced diabetic rats, we found that glomerular Klf2 expression was reduced in comparison with nondiabetic rats. However, normalization of hyperglycemia by insulin treatment increased Klf2 expression to a level higher than that of nondiabetic rats. Consistent with this, we found that Klf2 expression was suppressed by high glucose but increased by insulin in cultured endothelial cells. To determine the role of KLF2 in streptozotocin-induced diabetic nephropathy, we used endothelial cell-specific Klf2 heterozygous knockout mice and found that diabetic knockout mice developed more kidney/glomerular hypertrophy and proteinuria than diabetic wild-type mice. Glomerular expression of Vegfa, Flk1, and angiopoietin 2 increased, but expression of Flt1, Tie2, and angiopoietin 1 decreased, in diabetic knockout mice compared with diabetic wild-type mice. Glomerular expression of ZO-1, glycocalyx, and eNOS was also decreased in diabetic knockout compared with diabetic wild-type mice. These data suggest knockdown of Klf2 expression in the endothelial cells induced more endothelial cell injury. Interestingly, podocyte injury was also more prominent in diabetic knockout compared with diabetic wild-type mice, indicating a cross talk between these two cell types. Thus, KLF2 may play a role in glomerular endothelial cell injury in early diabetic nephropathy.
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