ArticleKidney international2012
Tubule-specific ablation of endogenous β-catenin aggravates acute kidney injury in mice.
Article in Kidney international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 130 papers.
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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.
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Who cites it
130 citing papers in PubMed, 220 citations in OpenAlex.
- Sustained tenascin-C activation drives AKI-to-CKD progression via the Wnt/β-catenin pathway.International urology and nephrology · 2026Article
- A skin-kidney neutrophil axis links ultraviolet exposure to renal angiogenesis and tissue remodeling in healthy and lupus kidneys.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Apoptosis and Cell Cycle Dysregulation in AmpligoJournal of xenobiotics · 2026Article
- Emerging therapeutic pipelines on kidney fibrosis: challenges in translational research.Journal of translational medicine · 2026Review
- Nanoparticles in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026Review
- Cisplatin-induced acute kidney injury is alleviated by BMSCs-derived exosome via mmu-miR-874-3p-mediated activation of the wnt/β-catenin signaling pathway.Regenerative therapy · 2025Article
- Inflammation in cardiovascular-kidney-metabolic syndrome: key roles and underlying mechanisms-a comprehensive review.Molecular and cellular biochemistry · 2025Review
- Fibrotic Disease: from Signaling Pathways and Biomarkers to Molecular Imaging.Molecular imaging and biology · 2025Review
- Exogenous spexin aggravates renal ischemia reperfusion injury and triggers toxicity in healthy kidneys.Frontiers of medicine · 2025Article
- Mechanisms of Acute Kidney Injury-Chronic Kidney Disease Transition: Unraveling Maladaptive Repair and Therapeutic Opportunities.Biomolecules · 2025Review
- Enzyme-Responsive Nanoparachute for Targeted miRNA Delivery: A Protective Strategy Against Acute Liver and Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Identification of potential hub genes and drugs in septic kidney injury: a bioinformatic analysis with preliminary experimental validation.Frontiers in medicine · 2025Article
- The Hippo Coactivator TAZ Exacerbates Cisplatin-Induced Acute Renal Injury.Kidney diseases (Basel, Switzerland) · 2024Article
- The crosstalk of Wnt/β-catenin signaling and p53 in acute kidney injury and chronic kidney disease.Kidney research and clinical practice · 2024Article
- β-catenin-inhibited Sumoylation modification of LKB1 and fatty acid metabolism is critical in renal fibrosis.Cell death & disease · 2024Article
- Targeted treatment of rat AKI induced by rhabdomyolysis using BMSC derived magnetic exosomes and its mechanism.Nanoscale advances · 2024Article
- Cell death induced by acute renal injury: a perspective on the contributions of accidental and programmed cell death.American journal of physiology. Renal physiology · 2024Review
- Proximal tubular FHL2, a novel downstream target of hypoxia inducible factor 1, is a protector against ischemic acute kidney injury.Cellular and molecular life sciences : CMLS · 2024Article
- Urinary cytokeratin 20 as a predictor for chronic kidney disease following acute kidney injury.JCI insight · 2024Article
- Dynamics of Wnt/β-catenin reporter activity throughout whole life in a naturally short-lived vertebrate.npj aging · 2024Article
70 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
β-Catenin is a unique intracellular protein functioning as an integral component of the cell-cell adherens complex and a principal signaling protein mediating canonical Wnt signaling. Little is known about its function in adult kidneys in the normal physiologic state or after acute kidney injury (AKI). To study this, we generated conditional knockout mice in which the β-catenin gene was specifically disrupted in renal tubules (Ksp-β-cat-/-). These mice were phenotypically normal with no appreciable defects in kidney morphology and function. In the absence of β-catenin, γ-catenin functionally substituted for it in E-cadherin binding, thereby sustaining the integrity of epithelial adherens junctions in the kidneys. In AKI induced by ischemia reperfusion or folic acid, the loss of tubular β-catenin substantially aggravated renal lesions. Compared with controls, Ksp-β-cat-/- mice displayed higher mortality, elevated serum creatinine, and more severe morphologic injury. Consistently, apoptosis was more prevalent in kidneys of the knockout mice, which was accompanied by increased expression of p53 and Bax, and decreased phosphorylated Akt and survivin. In vitro activation of β-catenin by Wnt1 or stabilization of β-catenin protected tubular epithelial cells from apoptosis, activated Akt, induced survivin, and repressed p53 and Bax expression. Hence, endogenous β-catenin is pivotal for renal tubular protection after AKI by promoting cell survival through multiple mechanisms.
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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.