ArticleJCI insight2022
Integrated single-cell transcriptomics and proteomics reveal cellular-specific responses and microenvironment remodeling in aristolochic acid nephropathy.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Beyond Tradition: An Integrated Toxicological, Ecological, and Public Health Perspective on Aristolochic Acids.Journal of applied toxicology : JAT · 2026Review
- Article
- ZBP1 promotes RIPK1-dependent apoptosis in aristolochic acid nephropathy.Zoological research · 2026Article
- Icaritin Ameliorates Cisplatin-Induced Mitochondrial Metabolic Dysfunction-Associated Nephrotoxicity and Synergistically Potentiates Its Antitumor Efficacy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fibrillin-1 Orchestrates a Pro-senescent Niche Driving Peritubular Endothelial Senescence via ZEB1/endothelin-1/β-catenin Signaling.International journal of biological sciences · 2026Article
- Integrating machine learning, deep learning, and docking to predict aristolochic acid A carcinogenesis.Frontiers in pharmacology · 2026Article
- From renal development to pathology: An analysis of the multilevel role of insulin‑like growth factor 2 (Review).Molecular medicine reports · 2026Review
- Integrated single-cell transcriptomics and proteomics elucidate the molecular mechanisms and detoxification strategy of rifampicin-induced hepatotoxicity.International journal of biological sciences · 2026Article
- Autophagy Related 5 Promotes Mitochondrial Fission and Inflammation via HSP90-HIF-1α-Mediated Glycolysis in Kidney Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Trajectory Inference for Single Cell Omics.ArXiv · 2025Article
- Exploring the pathogenesis of acute lung injury and its treatment through Traditional Chinese Medicine: a state-of-the-art review.Frontiers in pharmacology · 2025Review
- Renal tubular epithelial cell related partial epithelial-mesenchymal transition in AAⅠ induced renal fibrosis via Wnt7b/β-catenin signaling.Frontiers in pharmacology · 2025Article
- Review
- STEP: profiling cellular-specific targets and pathways of bioactive small molecules in tissuesChemical science · 2024Article
- Delineation of renal protein profiles in aristolochic acid I-induced nephrotoxicity in mice by label-free quantitative proteomics.Frontiers in pharmacology · 2024Article
- Identification and analysis of differently expressed transcription factors in aristolochic acid nephropathy.Environmental health and preventive medicine · 2024Article
- The Role of Immune Cells in DKD: Mechanisms and Targeted Therapies.Journal of inflammation research · 2024Review
- A single-cell landscape of triptolide-associated testicular toxicity in mice.Journal of pharmaceutical analysis · 2023Article
- Single-cell transcriptome analysis uncovers underlying mechanisms of acute liver injury induced by tripterygium glycosides tablet in mice.Journal of pharmaceutical analysis · 2023Article
- HDAC9-mediated epithelial cell cycle arrest in G2/M contributes to kidney fibrosis in male mice.Nature communications · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aristolochic acid nephropathy (AAN) is characterized by acute proximal tubule necrosis and immune cell infiltration, contributing to the global burden of chronic kidney disease and urothelial cancer. Although the proximal tubule has been defined as the primary target of aristolochic acids I (AAI), the mechanistic underpinning of gross renal deterioration caused by AAI has not been explicitly explained, prohibiting effective therapeutic intervention. To this point, we employed integrated single-cell RNA-Seq, bulk RNA-Seq, and mass spectrometry-based proteomics to analyze the mouse kidney after acute AAI exposure. Our results reveal a dramatic reduction of proximal tubule epithelial cells, associated with apoptotic and inflammatory pathways, indicating permanent damage beyond repair. We found the enriched development pathways in other nephron segments, suggesting activation of reparative programs triggered by AAI. The divergent response may be attributed to the segment-specific distribution of organic anion channels along the nephron, including OAT1 and OAT3. Moreover, we observed dramatic activation and recruitment of cytotoxic T and macrophage M1 cells, highlighting inflammation as a principal contributor to permanent renal injury. Ligand-receptor pairing revealed that critical intercellular crosstalk underpins damage-induced activation of immune cells. These results provide potentially novel insight into the AAI-induced kidney injury and point out possible pathways for future therapeutic intervention.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.