ArticleInternational journal of medical sciences2022
Differential lipidomics of HK-2 cells and exosomes under high glucose stimulation.
Article in International journal of medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Renal Lipid Alterations From Diabetes to Early-Stage Diabetic Kidney Disease and Mitophagy: Focus on Cardiolipin.Journal of cellular and molecular medicine · 2025Article
- Effects and Mechanisms of Extracellular Vesicles in Different Models of Acute Kidney Injury.Stem cells international · 2025Review
- Role of Exosomal miR-205-5p Cargo in Angiogenesis and Cell Migration.International journal of molecular sciences · 2024Article
- The role of intercellular communication in diabetic nephropathy.Frontiers in immunology · 2024Review
- Enhanced Levels of Glycosphingolipid GM3 Delay the Progression of Diabetic Nephropathy.International journal of molecular sciences · 2023Article
- Oxidative Stress and Lipid Dysregulation in Lipid Droplets: A Connection to Chronic Kidney Disease Revealed in Human Kidney Cells.Antioxidants (Basel, Switzerland) · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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Abstract
Abnormal cellular lipid metabolism has a very important role in the occurrence and progression of diabetic kidney disease (DKD). However, the lipid composition and differential expression by high glucose stimulation of renal tubular cells and their exosomes, which is a vital part of the development of DKD, are largely unknown. In this study, based on targeted lipid analysis by isotope labeling and tandem mass spectrometry, a total of 421 and 218 lipid species were quantified in HK-2 cells and exosomes, respectively. More importantly, results showed that GM3 d18:1/22:0, GM3 d18:1/16:0, GM3 d18:0/16:0, GM3 d18:1/22:1 were significantly increased, while LPE18:1, LPE, CL66:4 (16:1), BMP36:3, CL70:7 (16:1), CL74:8 (16:1) were significantly decreased in high glucose-stimulated HK-2 cells. Also, PG36:1, FFA22:5, PC38:3, SM d18:1/16:1, CE-16:1, CE-18:3, CE-20:5, and CE-22:6 were significantly increased, while GM3 d18:1/24:1, GM3 were significantly decreased in exosomes secreted by high glucose-stimulated HK-2 cells. Furthermore, TAG, PC, CL were decreased significantly in the exosomes comparing with the HK-2 cells, and LPA18:2, LPI22:5, PG32:2, FFA16:1, GM3 d18:1/18:1, GM3 d18:1/20:1, GM3 d18:0/20:0, PC40:6p, TAG52:1(18:1), TAG52:0(18:0), CE-20:5, CE-20:4, CE-22:6 were only found in exosomes. In addition, the expression of PI4P in HK-2 cells decreased under a high glucose state. These data may be useful to provide new targets for exploring the mechanisms of DKD.
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