ArticleScientific reports2018
Aristolochic acid I determine the phenotype and activation of macrophages in acute and chronic kidney disease.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Enhancement of angiotensin II type 1 receptor-associated protein suppresses kidney inflammation in a mouse model of aristolochic acid nephropathy.Scientific reports · 2025Article
- Kidney immunology from pathophysiology to clinical translation.Nature reviews. Immunology · 2025Review
- The Double-Edge Sword of Natural Phenanthrenes in the Landscape of Tumorigenesis.Molecules (Basel, Switzerland) · 2025Review
- Chronic kidney disease amplifies severe kidney injury and mortality in a mouse model of skin arsenical exposure.American journal of physiology. Renal physiology · 2025Article
- Bidirectional Interaction Between Chronic Kidney Disease andJournal of immunology research · 2025Article
- Unveiling correlations between aristolochic acids and liver cancer: spatiotemporal heterogeneity phenomenon.Chinese medicine · 2024Review
- Dissection of cellular and molecular mechanisms of aristolochic acid-induced hepatotoxicity via single-cell transcriptomics.Precision clinical medicine · 2022Article
- Aristolochic acid-induced nephropathy is attenuated in mice lacking the neutral amino acid transporter BAmerican journal of physiology. Renal physiology · 2022Article
- Integrated single-cell transcriptomics and proteomics reveal cellular-specific responses and microenvironment remodeling in aristolochic acid nephropathy.JCI insight · 2022Article
- Macrophage-derived, LRG1-enriched extracellular vesicles exacerbate aristolochic acid nephropathy in a TGFβR1-dependent manner.Cell biology and toxicology · 2022Article
- Macrophage interferon regulatory factor 4 deletion ameliorates aristolochic acid nephropathy via reduced migration and increased apoptosis.JCI insight · 2022Article
- Article
- Bioinformatics analysis of biomarkers of aristolochic acid-induced early nephrotoxicity in embryonic stem cells.Experimental and therapeutic medicine · 2021Article
- Nephrotoxicity of Herbal Products in Europe-A Review of an Underestimated Problem.International journal of molecular sciences · 2021Review
- The targets of β-sitosterol as a novel therapeutic against cardio-renal complications in acute renal ischemia/reperfusion damage.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Ibudilast Attenuates Folic Acid-Induced Acute Kidney Injury by Blocking Pyroptosis Through TLR4-Mediated NF-κB and MAPK Signaling Pathways.Frontiers in pharmacology · 2021Article
- Only Hyperuricemia with Crystalluria, but not Asymptomatic Hyperuricemia, Drives Progression of Chronic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2020Article
- Aristolochic Acid-Induced Nephrotoxicity: Molecular Mechanisms and Potential Protective Approaches.International journal of molecular sciences · 2020Review
- Article
- Protective Effects of Melatonin Against Aristolochic Acid-Induced Nephropathy in Mice.Biomolecules · 2019Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute and chronic kidney injuries are multifactorial traits that involve various risk factors. Experimental animal models are crucial to unravel important aspects of injury and its pathophysiological mechanisms. Translating knowledge obtained from experimental approaches into clinically useful information is difficult; therefore, significant attention needs to be paid to experimental procedures that mimic human disease. Herein, we compared aristolochic acid I (AAI) acute and chronic kidney injury model with unilateral ischemic-reperfusion injury (uIRI), cisplatin (CP)- or folic acid (FA)-induced renal damage. The administration of AAI showed significant changes in serum creatinine and BUN upon CKD. The number of neutrophils and macrophages were highly increased as well as AAI-induced CKD characterized by loss of tubular epithelial cells and fibrosis. The in vitro and in vivo data indicated that macrophages play an important role in the pathogenesis of AA-induced nephropathy (AAN) associated with an excessive macrophage accumulation and an alternative activated macrophage phenotype. Taken together, we conclude that AA-induced injury represents a suitable and relatively easy model to induce acute and chronic kidney injury. Moreover, our data indicate that this model is appropriate and superior to study detailed questions associated with renal macrophage phenotypes.
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