ArticleKidney international2024
Chronic kidney disease in a murine model of non-alcoholic steatohepatitis (NASH).
Article in Kidney international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- The case for cardiovascular-kidney-liver-metabolic syndrome.Nature reviews. Nephrology · 2026Article
- STK40 inhibits profibrotic Arg1Acta pharmacologica Sinica · 2026Article
- Peroxisomes in Liver Diseases: From Metabolite Quality Control to Inter-Organelle and Inter-Organ Signaling.Biomolecules · 2026Review
- Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models.Nature reviews. Gastroenterology & hepatology · 2026Review
- Cross-sectional and longitudinal associations between fatty liver index and kidney function using updated MASLD and CKD-EPI 2021 definitions: a population-based study with region-specific cutoffs.European journal of medical research · 2025Article
- Noninvasive assessment of metabolic syndrome-related renal injury using magnetic resonance imaging fat fraction and apparent diffusion coefficient: A cross-sectional study.The Journal of international medical research · 2025Article
- Disorder of phospholipid metabolism in the renal cortex and medulla contributes to acute tubular necrosis in mice after cantharidin exposure using integrative lipidomics and spatial metabolomics.Journal of pharmaceutical analysis · 2025Article
- Liver fibrosis progression analyzed with AI predicts renal decline.JHEP reports : innovation in hepatology · 2025Article
- Advances in Extracellular Matrix-Associated Diagnostics and Therapeutics.Journal of clinical medicine · 2025Review
- New insights into kidney crosstalk with distant organs.Nature reviews. Nephrology · 2025Article
- Altered mitochondrial function: a clue therapeutic strategies between metabolic dysfunction-associated steatotic liver disease and chronic kidney disease?Frontiers in nutrition · 2025Review
- Association between non-high-density lipoprotein cholesterol-to-high-density lipoprotein cholesterol ratio and macroalbuminuria: evidence from NHANES 1999-2018.Frontiers in endocrinology · 2025Article
- Collagen-targeted protein nanomicelles for the imaging of non-alcoholic steatohepatitis.Acta biomaterialia · 2024Article
- Development of Liver Fibrosis Represented by the Fibrosis-4 Index Is a Specific Risk Factor for Tubular Injury in Individuals with Type 2 Diabetes.Biomedicines · 2024Article
- Emerging Roles of Xanthine Oxidoreductase in Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Molecular mechanism of renal lipid accumulation in diabetic kidney disease.Journal of cellular and molecular medicine · 2024Review
- Normal and Dysregulated Sphingolipid Metabolism: Contributions to Podocyte Injury and Beyond.Cells · 2024Review
- Mechanisms of hepatic and renal injury in lipid metabolism disorders in metabolic syndrome.International journal of biological sciences · 2024Review
- Systemic impacts of metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) on heart, muscle, and kidney related diseases.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Clinical studies suggest that non-alcoholic steatohepatitis (NASH) is an independent risk factor for chronic kidney disease (CKD), but causality and mechanisms linking these two major diseases are lacking. To assess whether NASH can induce CKD, we have characterized kidney function, histological features, transcriptomic and lipidomic profiles in a well-validated murine NASH model. Mice with NASH progressively developed significant podocyte foot process effacement, proteinuria, glomerulosclerosis, tubular epithelial cell injury, lipid accumulation, and interstitial fibrosis. The progression of kidney fibrosis paralleled the severity of the histologic NASH-activity score. Significantly, we confirmed the causal link between NASH and CKD by orthotopic liver transplantation, which attenuated proteinuria, kidney dysfunction, and fibrosis compared with control sham operated mice. Transcriptomic analysis of mouse kidney cortices revealed differentially expressed genes that were highly enriched in mitochondrial dysfunction, lipid metabolic process, and insulin signaling pathways in NASH-induced CKD. Lipidomic analysis of kidney cortices further revealed that phospholipids and sphingolipids were the most significantly changed lipid species. Notably, we found similar kidney histological changes in human NASH and CKD. Thus, our results confirm a causative role of NASH in the development of CKD, reveal potential pathophysiologic mechanisms of NASH-induced kidney injury, and established a valuable model to study the pathogenesis of NASH-associated CKD. This is an important feature of fatty liver disease that has been largely overlooked but has clinical and prognostic importance.
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