ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021
Gene expression profiles of diabetic kidney disease and neuropathy in eNOS knockout mice: Predictors of pathology and RAS blockade effects.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- NONcNZO10/LtJ and TALLY-HO/JngJ Mice as Novel Models of Diabetic Peripheral Neuropathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024Review
- Transcriptomic profiling of sciatic nerves and dorsal root ganglia reveals site-specific effects of prediabetic neuropathy.Translational research : the journal of laboratory and clinical medicine · 2024Article
- Transcriptomic analysis of diabetic kidney disease and neuropathy in mouse models of type 1 and type 2 diabetes.Disease models & mechanisms · 2023Article
- New perspectives in diabetic neuropathy.Neuron · 2023Review
- Rodent models to study type 1 and type 2 diabetes induced human diabetic nephropathy.Molecular biology reports · 2023Review
- Single-cell RNA-seq uncovers novel metabolic functions of Schwann cells beyond myelination.Journal of neurochemistry · 2023Article
- Identification of Immune Infiltration and the Potential Biomarkers in Diabetic Peripheral Neuropathy through Bioinformatics and Machine Learning Methods.Biomolecules · 2022Article
- The Michigan O'Brien Kidney Research Center: transforming translational kidney research through systems biology.American journal of physiology. Renal physiology · 2022Review
- Endothelial Nitric Oxide Synthase (eNOS) and the Cardiovascular System: in Physiology and in Disease States.American journal of biomedical science & research · 2022Article
- Advances in diet-induced rodent models of metabolically acquired peripheral neuropathy.Disease models & mechanisms · 2021Article
- Renin-angiotensin system inhibition reverses the altered triacylglycerol metabolic network in diabetic kidney disease.Metabolomics : Official journal of the Metabolomic Society · 2021Article
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
Abstract
Diabetic kidney disease (DKD) and diabetic peripheral neuropathy (DPN) are two common diabetic complications. However, their pathogenesis remains elusive and current therapies are only modestly effective. We evaluated genome-wide expression to identify pathways involved in DKD and DPN progression in db/db eNOS-/- mice receiving renin-angiotensin-aldosterone system (RAS)-blocking drugs to mimic the current standard of care for DKD patients. Diabetes and eNOS deletion worsened DKD, which improved with RAS treatment. Diabetes also induced DPN, which was not affected by eNOS deletion or RAS blockade. Given the multiple factors affecting DKD and the graded differences in disease severity across mouse groups, an automatic data analysis method, SOM, or self-organizing map was used to elucidate glomerular transcriptional changes associated with DKD, whereas pairwise bioinformatic analysis was used for DPN. These analyses revealed that enhanced gene expression in several pro-inflammatory networks and reduced expression of development genes correlated with worsening DKD. Although RAS treatment ameliorated the nephropathy phenotype, it did not alter the more abnormal gene expression changes in kidney. Moreover, RAS exacerbated expression of genes related to inflammation and oxidant generation in peripheral nerves. The graded increase in inflammatory gene expression and decrease in development gene expression with DKD progression underline the potentially important role of these pathways in DKD pathogenesis. Since RAS blockers worsened this gene expression pattern in both DKD and DPN, it may partly explain the inadequate therapeutic efficacy of such blockers.
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