ArticleKidney international2019
Wnt/β-catenin signaling mediates both heart and kidney injury in type 2 cardiorenal syndrome.
Article in Kidney international, 2019. 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 70 papers, 1 of them a synthesis that pooled it.
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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
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.
- Cardiorenal Associations in Preclinical Modeling: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2026Pooled it
- Combined podocyte, fibrotic and echocardiographic correlates of an operationally defined subclinical cardiorenal phenotype in chronic kidney disease: an exploratory study.Renal failure · 2026Observational
- An Integrated Therapeutic Strategy for Cardiorenal Syndrome to Target Oxidative Stress, Inflammation, and Fibrosis.Reviews in cardiovascular medicine · 2026Review
- Decoding cardiorenal crosstalk: Intercellular communication mechanisms and therapeutic insights in cardiorenal syndrome.iScience · 2026Review
- Challenges and opportunities for ginseng-based medicines in treating cardiac fibrosis from mechanistic insights to clinical translation.Chinese herbal medicines · 2026Review
- Icariin Attenuates Renal Injury in Streptozotocin-Induced Diabetic Rats with and Without Adenine-Induced Chronic Kidney Disease.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Circular RNA-mediated regulation of key signaling pathways in cardiovascular diseases: a review.Journal of advanced research · 2026Review
- RNF220 mediates K63-linked polyubiquitination of STAT3 and aggravates pathological cardiac hypertrophy.Cell death and differentiation · 2026Article
- Montelukast attenuates diclofenac sodium-induced cardiotoxicity in male rats via targeting Wnt/β-catenin pathway.Scientific reports · 2026Article
- Prognostic utility of Wnt/β-catenin signaling pathway biomarkers in predicting outcomes of patients with ST-segment elevation myocardial infarction.Frontiers in cardiovascular medicine · 2026Article
- Review
- Homocysteine promotes cardiomyocyte hypertrophy through inhibiting β-catenin/ FUNDC1 mediated mitophagy.Scientific reports · 2025Article
- Cardiorenal syndrome: clinical diagnosis, molecular mechanisms and therapeutic strategies.Acta pharmacologica Sinica · 2025Review
- Plasma Dickkopf-1 Levels Are Associated with Chronic Kidney Disease.Metabolites · 2025Article
- The true cost of phosphate control in chronic kidney disease.Clinical kidney journal · 2025Article
- The mechanism of enterogenous toxin methylmalonic acid aggravating calcium-phosphorus metabolic disorder in uremic rats by regulating the Wnt/β-catenin pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Acute kidney injury after myocardial infarction: prognostic implications via dual robust methods.Frontiers in medicine · 2025Article
- Decoding Sepsis: Unraveling Key Signaling Pathways for Targeted Therapies.Research (Washington, D.C.) · 2025Review
- Global trends and disparities in the burden of heart failure caused by chronic kidney disease: an analysis of the global burden of disease study 2021.Frontiers in medicine · 2025Article
- Wnt Signaling Inhibitors as Therapeutic Approach in Ischemic Heart Disease.Molecules (Basel, Switzerland) · 2024Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
In type 2 cardiorenal syndrome, chronic heart failure is thought to cause or promote chronic kidney disease; however, the underlying mechanisms remain poorly understood. We investigated the role of Wnt signaling in heart and kidney injury in a mouse model of cardiac hypertrophy and heart failure induced by transverse aortic constriction (TAC). At 8 weeks after TAC, cardiac hypertrophy, inflammation, and fibrosis were prominent, and echocardiography confirmed impaired cardiac function. The cardiac lesions were accompanied by upregulation of multiple Wnt ligands and activation of β-catenin, as well as activation of the renin-angiotensin system (RAS). Wnt3a induced multiple components of the RAS in primary cardiomyocytes and cardiac fibroblasts in vitro. TAC also caused proteinuria and kidney fibrosis, accompanied by klotho depletion and β-catenin activation in the kidney. Pharmacologic blockade of β-catenin with a small molecule inhibitor or the RAS with losartan ameliorated cardiac injury, restored heart function, and mitigated the renal lesions. Serum from TAC mice was sufficient to activate β-catenin and trigger tubular cell injury in vitro, indicating a role for circulating factors. Multiple inflammatory cytokines were upregulated in the circulation of TAC mice, and tumor necrosis factor-α was able to inhibit klotho, induce β-catenin activation, and cause tubular cell injury in vitro. These studies identify Wnt/β-catenin signaling as a common pathogenic mediator of heart and kidney injury in type 2 cardiorenal syndrome after TAC. Targeting this pathway could be a promising therapeutic strategy to protect both organs in cardiorenal syndrome.
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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 Socratic graph.