ArticleAmerican journal of physiology. Endocrinology and metabolism2021
Increased vascular permeability and severe renal tubular damage after ischemia-reperfusion injury in mice lacking adiponectin or T-cadherin.
Article in American journal of physiology. Endocrinology and metabolism, 2021. 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, 34 citations in OpenAlex.
- Adiponectin and aging: Mechanistic insights, clinical paradox, and therapeutic horizons.Ageing research reviews · 2026Review
- T‑cadherin and its impact on human diseases (Review).Molecular medicine reports · 2026Review
- 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
- Article
- Downregulation of sST2, a decoy receptor for interleukin-33, enhances subcutaneous tumor growth in murine pancreatic cancer cells.FEBS open bio · 2025Article
- Exploring the impact of ADIPOQ gene variants on plasma adiponectin levels and oxidative stress in type 2 diabetes mellitus and diabetic nephropathy in South Indian population: a case-control study.Diabetology international · 2025Article
- T-Cadherin (International journal of molecular sciences · 2025Review
- Emerging Frontiers in acute kidney injury: The role of extracellular vesicles.Bioactive materials · 2025Review
- Identification of an anti-inflammatory action of exosome release in P2YFrontiers in pharmacology · 2025Article
- Metabolic Syndrome, Kidney-Related Adiposity, and Kidney Microcirculation: Unraveling the Damage.Biomedicines · 2024Review
- Obesity aggravates acute kidney injury resulting from ischemia and reperfusion in mice.Scientific reports · 2024Article
- Pharmacological HIF-1 activation upregulates extracellular vesicle production synergistically with adiponectin through transcriptional induction and protein stabilization of T-cadherin.Scientific reports · 2024Article
- Exosomes Highlight Future Directions in the Treatment of Acute Kidney Injury.International journal of molecular sciences · 2023Review
- Endogenous renal adiponectin drives gluconeogenesis through enhancing pyruvate and fatty acid utilization.Nature communications · 2023Article
- T-Cadherin Deficiency Is Associated with Increased Blood Pressure after Physical Activity.International journal of molecular sciences · 2023Article
- Platelet ITGA2B inhibits caspase-8 and Rip3/Mlkl-dependent platelet death though PTPN6 during sepsis.iScience · 2023Article
- The Role of Adipokines in the Pathogenesis of Psoriasis.International journal of molecular sciences · 2023Review
- The Relationship between Serum Adiponectin, Urinary Albumin/Creatinine Ratio and Type 2 Diabetes: A Population-Based Cross-Sectional Study.Journal of clinical medicine · 2022Article
- Time-Series Change of Serum Soluble T-Cadherin Concentrations and Its Association with Creatine Kinase-MB Levels in ST-Segment Elevation Myocardial Infarction.Journal of atherosclerosis and thrombosis · 2022Observational
- Extracellular Vesicles as an Endocrine Mechanism Connecting Distant Cells.Molecules and cells · 2022Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adiponectin (APN) is a circulating protein specifically produced by adipocytes. Native APN specifically binds to T-cadherin, a glycosylphosphatidylinositol-anchored protein, mediating the exosome-stimulating effects of APN in endothelial, muscle, and mesenchymal stem cells. It was previously reported that APN has beneficial effects on kidney diseases, but the role of T-cadherin has not been clarified yet. Here, our immunofluorescence study indicated the existence of both T-cadherin and APN protein in pericytes, subsets of tissue-resident mesenchymal stem/progenitor cells positive for platelet-derived growth factor receptor β (PDGFRβ), surrounding peritubular capillaries. In an acute renal ischemia-reperfusion (I/R) model, T-cadherin-knockout (Tcad-KO) mice, similar to APN-KO mice, exhibited the more progressive phenotype of renal tubular damage and increased vascular permeability than wild-type mice. In addition, in response to I/R-injury, the renal PDGFRβ-positive cell area increased in wild-type mice, but opposingly decreased in both Tcad-KO and APN-KO mice, suggesting severe pericyte loss. Mouse primary pericytes also expressed T-cadherin. APN promoted exosome secretion in a T-cadherin-dependent manner. Such exosome production from pericytes may play an important role in maintaining the capillary network and APN-mediated inhibition of renal tubular injury. In summary, our study suggested that APN protected the kidney in an acute renal injury model by binding to T-cadherin.
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