ArticleKidney international2012
Targeted proximal tubule injury triggers interstitial fibrosis and glomerulosclerosis.
Article in Kidney international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 276 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
276 citing papers in PubMed, 1 synthesis or guideline pooled it, 463 citations in OpenAlex.
- Metformin for preventing the progression of chronic kidney disease.The Cochrane database of systematic reviews · 2024 · on this mapPooled it
- Fibrinogen-like protein 2-complement C3 interaction exacerbates tubular inflammation in acute kidney injury by elevating complement C3a levels.Renal failure · 2026Article
- Elevated glucose in kidney organoids induces tissue-intrinsic inflammation driving epithelial detachment.Stem cell reports · 2026Article
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Iron-catalyzed oxidative stress reveals an exposome-related ferroptosis-resistant karyomegalic niche in BRCA1-linked renal carcinogenesis.Redox biology · 2026Article
- Tackling aging and chronic disease: How space exploration and the 'chameleon effect' of pharmaceuticals can lead the way.Experimental physiology · 2026Review
- Apical proximal tubule fatty acid uptake-generated ceramides cause endoplasmic reticulum stress from altered membrane fluidity.JCI insight · 2026Article
- Early detection of proteinuria to prevent kidney fibrosis and progression to kidney failure: lessons from the School Urine Screening Program in Japan.Pediatric nephrology (Berlin, Germany) · 2026Review
- Targeting YAP1-Mediated Tubular Cell Senescence to Attenuate Maladaptive Repair and Fibrotic Transition After Acute Kidney Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Renal Tubule Cell-SpecificHypertension (Dallas, Tex. : 1979) · 2026Article
- A multi-omics map of diabetic nephropathy reveals c-Jun as a driver of tubular injury and metabolic stress.bioRxiv : the preprint server for biology · 2026Article
- Review
- Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026Review
- High-Dose Voclosporin Protects Against Acute Kidney Injury via Regnase-2-Mediated NGAL MRNA Decay.International journal of molecular sciences · 2026Article
- Tubular Epithelia-Specific Deletion of MCP-1 Does Not Afford Protection Against Adriamycin-Induced Kidney Injury.International journal of molecular sciences · 2026Article
- Pyruvate Dehydrogenase and Cellular Metabolism in Calcineurin Inhibitor-Induced Kidney Fibrosis.Journal of the American Society of Nephrology : JASN · 2026Article
- Inhaled Halogen-Induced Oxidative Renal Damage and Dysfunction: A Lung Heart Kidney Axis.Comprehensive Physiology · 2026Article
- Advances in the Targeted Drug Delivery System for Renal Fibrosis.International journal of nanomedicine · 2026Review
- SPARC Drives Tubulointerstitial Fibrosis through Regulating the CBP-DOT1L Pathway.International journal of biological sciences · 2026Article
- Inflammation-related lncRNAs in the regulation of kidney injuries; special emphasis on novel lncRNA-based delivery platforms.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
216 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
Chronic kidney disease (CKD) remains one of the leading causes of death in the developed world, and acute kidney injury (AKI) is now recognized as a major risk factor in its development. Understanding the factors leading to CKD after acute injury are limited by current animal models of AKI, which concurrently target various kidney cell types including epithelial, endothelial, and inflammatory cells. Here, we developed a mouse model of kidney injury using the Six2-Cre-LoxP technology to selectively activate expression of the simian diphtheria toxin (DT) receptor in renal epithelia derived from the metanephric mesenchyme. By adjusting the timing and dose of DT, a highly selective model of tubular injury was created to define the acute and chronic consequences of isolated epithelial injury. The DT-induced sublethal tubular epithelial injury was confined to the S1 and S2 segments of the proximal tubule rather than being widespread in the metanephric mesenchyme-derived epithelial lineage. Acute injury was promptly followed by inflammatory cell infiltration and robust tubular cell proliferation, leading to complete recovery after a single toxin insult. In striking contrast, three insults to renal epithelial cells at 1-week intervals resulted in maladaptive repair with interstitial capillary loss, fibrosis, and glomerulosclerosis, which was highly correlated with the degree of interstitial fibrosis. Thus, selective epithelial injury can drive the formation of interstitial fibrosis, capillary rarefaction, and potentially glomerulosclerosis, substantiating a direct role for damaged tubule epithelium in the pathogenesis of CKD.
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What OpenQuestion holds
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.