ArticleThe Journal of clinical investigation2010
T-cadherin is critical for adiponectin-mediated cardioprotection in mice.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
184 citing papers in PubMed, 341 citations in OpenAlex.
- Adipokines as Regulators of Nitric Oxide Synthase Isoforms Across Organs: Emerging Implications for Gastrointestinal Motility.International journal of molecular sciences · 2026Review
- Neonatal hyperoxia promotes macrophage senescence and lung injury via a p38MAPK-dependent secretome.American journal of respiratory cell and molecular biology · 2026Article
- Regulatory Roles of Adiponectin in Animal Reproduction: Molecular Insights from the Hypothalamic-Pituitary-Gonadal Axis.Biomolecules · 2026Review
- T‑cadherin and its impact on human diseases (Review).Molecular medicine reports · 2026Review
- Soluble T-Cadherin: A Novel Biomarker for Fluid Resuscitation in Burn Patients-A Single-Center Retrospective Observational Study.Shock (Augusta, Ga.) · 2026Observational
- T-cadherin, a major adiponectin binding partner, suppresses ERK signaling in metabolic tissues.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- T-cadherin as a potential novel regulator of intestinal inflammation and fibrosis.Frontiers in physiology · 2026Review
- Gender differences in adiponectin levels among obese individuals and their association with cardiovascular disease.Frontiers in cell and developmental biology · 2026Review
- Revisiting the multiple roles of T-cadherin and adiponectin in cardiovascular disease: from receptor function to exosome-mediated therapeutic potential.Ewha medical journal · 2026Article
- Predictive Value of Adiponectin for Long-Term MACEs in Non-Diabetic STEMI Patients.Journal of clinical medicine · 2025Article
- T-Cadherin Finetunes Proliferation-Differentiation During Adipogenesis via PI3K-AKT Signaling Pathway.International journal of molecular sciences · 2025Article
- Disuse-induced muscle-type specific alterations and adiponectin pathway response in male mice.Physiological reports · 2025Article
- Immune Dysregulation Connecting Type 2 Diabetes and Cardiovascular Complications.Life (Basel, Switzerland) · 2025Review
- Harnessing adiponectin for sepsis: current knowledge, clinical insights and future therapies.Critical care (London, England) · 2025Review
- T-Cadherin (International journal of molecular sciences · 2025Review
- Unravelling the Adiponectin Hallmark and Exploring the Therapeutic Potential of Its Receptor Agonists in Cancer Metabolic Reprogramming.Biomolecules · 2025Review
- Adiponectin and Adiponectin Receptors in Atherosclerosis.Endocrine reviews · 2025Review
- New evidence for T-cadherin in COVID-19 pathogenesis, endothelial dysfunction, and lung fibrosis.Frontiers in cell and developmental biology · 2025Article
- Adiponectin receptor T-cadherin emerges as a novel regulator of adipose stem cell quiescence and adipogenesis.Frontiers in cell and developmental biology · 2025Article
- Identification of an anti-inflammatory action of exosome release in P2YFrontiers in pharmacology · 2025Article
124 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The circulating, adipocyte-secreted hormone adiponectin (APN) exerts protective effects on the heart under stress conditions. The receptors binding APN to cardiac tissue, however, have remained elusive. Here, we report that the glycosyl phosphatidylinositol–anchored cell surface glycoprotein T-cadherin (encoded by Cdh13) protects against cardiac stress through its association with APN in mice. We observed extensive colocalization of T-cadherin and APN on cardiomyocytes in vivo. In T-cadherin-deficient mice, APN failed to associate with cardiac tissue, and its levels dramatically increased in the circulation. Pressure overload stress resulted in exacerbated cardiac hypertrophy in T-cadherin-null mice and paralleled corresponding defects in mice lacking APN. During ischemia-reperfusion injury, the absence of T-cadherin increased infarct size similar to that in APN-null mice. Myocardial AMPK is a major downstream protective signaling target of APN. In both cardiac hypertrophy and ischemia-reperfusion models, T-cadherin was necessary for APN-dependent AMPK phosphorylation. In APN-null mice, recombinant adenovirus-expressed APN reduced exaggerated hypertrophy and infarct size and restored AMPK phosphorylation as previously reported. In contrast, rescue was ineffective in mice lacking T-cadherin in addition to APN. These data suggest that T-cadherin protects from stress-induced pathological cardiac remodeling by binding APN and activating its cardioprotective functions.
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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.