ReviewFrontiers in medicine2022
Experimental Aristolochic Acid Nephropathy: A Relevant Model to Study AKI-to-CKD Transition.
Review in Frontiers in medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 46 citations in OpenAlex.
- Pregnane X receptor mitigates aristolochic acid-induced acute kidney injury via p53 ubiquitination.Renal failure · 2026Article
- Beyond Tradition: An Integrated Toxicological, Ecological, and Public Health Perspective on Aristolochic Acids.Journal of applied toxicology : JAT · 2026Review
- Pharmacologic disruption of HuR-RNA interactions prevents maladaptive tubular repair and AKI-to-CKD progression.American journal of physiology. Renal physiology · 2026Article
- TRAP5 Inhibition Targeting Scar-Associated Macrophages Ameliorates Acute Kidney Injury to Chronic Kidney Disease Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ZBP1 promotes RIPK1-dependent apoptosis in aristolochic acid nephropathy.Zoological research · 2026Article
- Platelet dysfunction in chronic kidney disease arises from bone marrow remodeling and megakaryocyte reprogramming.Blood advances · 2026Article
- Linagliptin loaded chitosan nanoparticles for the efficient therapy of renal fibrosis.Frontiers in pharmacology · 2026Article
- Nephroprotective Plant Species Used in Brazilian Traditional Medicine for Renal Diseases: Ethnomedical, Pharmacological, and Chemical Insights.Plants (Basel, Switzerland) · 2025Review
- Integrated transcriptomic and single-cell RNA-seq analysis identifies CLCNKB, KLK1 and PLEKHA4 as key gene of AKI-to-CKD progression.Frontiers in immunology · 2025Article
- Renal tubular epithelial cell related partial epithelial-mesenchymal transition in AAⅠ induced renal fibrosis via Wnt7b/β-catenin signaling.Frontiers in pharmacology · 2025Article
- Dynamic changes in sleep architecture in a mouse model of acute kidney injury transitioning to chronic kidney disease.Frontiers in neuroscience · 2025Article
- Western diet exacerbates a murine model of Balkan nephropathy.American journal of physiology. Renal physiology · 2025Article
- Chronic Kidney Disease of Unknown Etiology: A Global Health Threat in Rural Agricultural Communities-Prevalence, Suspected Causes, Mechanisms, and Prevention Strategies.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024Review
- A novel model of cardiovascular-kidney-metabolic syndrome combining unilateral nephrectomy and high-salt-sugar-fat diet in mice.Lab animal · 2024Article
- C/EBPδ Mediates Immunity to Renal Autoinflammatory Disorders in a Stage-specific Manner.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Cognate antigen-independent differentiation of resident memory T cells in chronic kidney disease.American journal of physiology. Renal physiology · 2024Article
- Evaluating the Safety of Herbal Medicine on Renal Function: A Comprehensive Analysis from Six Randomized Controlled Trials Conducted with Four Formulations from Traditional Korean Medicine.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Macrophages polarization in renal inflammation and fibrosis animal models (Review).Molecular medicine reports · 2024Review
- SGLT2 inhibitor dapagliflozin protects the kidney in a murine model of Balkan nephropathy.American journal of physiology. Renal physiology · 2024Article
- New Insights into the Nephroprotective Potential of Lercanidipine.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aristolochic acid nephropathy (AAN) is a progressive tubulointerstitial nephritis caused by the intake of aristolochic acids (AA) contained in Chinese herbal remedies or contaminated food. AAN is characterized by tubular atrophy and interstitial fibrosis, characterizing advanced kidney disease. It is established that sustained or recurrent acute kidney injury (AKI) episodes contribute to the progression of CKD. Therefore, the study of underlying mechanisms of AA-induced nephrotoxicity could be useful in understanding the complex AKI-to-CKD transition. We developed a translational approach of AKI-to-CKD transition by reproducing human AAN in rodent models. Indeed, in such models, an early phase of acute tubular necrosis was rapidly followed by a massive interstitial recruitment of activated monocytes/macrophages followed by cytotoxic T lymphocytes, resulting in a transient AKI episode. A later chronic phase was then observed with progressive tubular atrophy related to dedifferentiation and necrosis of tubular epithelial cells. The accumulation of vimentin and αSMA-positive cells expressing TGFβ in interstitial areas suggested an increase in resident fibroblasts and their activation into myofibroblasts resulting in collagen deposition and CKD. In addition, we identified 4 major actors in the AKI-to-CKD transition: (1) the tubular epithelial cells, (2) the endothelial cells of the interstitial capillary network, (3) the inflammatory infiltrate, and (4) the myofibroblasts. This review provides the most comprehensive and informative data we were able to collect and examines the pending questions.
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Registered trials
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 OpenQuestion graph.