ArticleCardiovascular diabetology2017
T-cadherin deficiency increases vascular vulnerability in T2DM through impaired NO bioactivity.
Article in Cardiovascular diabetology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 12 citations in OpenAlex.
- 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
- 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
- Decoding the enigmatic role of T-cadherin in tumor angiogenesis.Frontiers in immunology · 2025Review
- T-Cadherin Deficiency Is Associated with Increased Blood Pressure after Physical Activity.International journal of molecular sciences · 2023Article
- Role of adiponectin in osteoarthritis.Frontiers in cell and developmental biology · 2022Review
- Vascular endothelial adiponectin signaling across the life span.American journal of physiology. Heart and circulatory physiology · 2022Review
- Endothelial dysfunction and platelet hyperactivity in type 2 diabetes mellitus: molecular insights and therapeutic strategies.Cardiovascular diabetology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundEndothelial dysfunction plays a critical role in the development of type 2 diabetes (T2DM). T-cadherin (T-cad) has gained recognition as a regulator of endothelial cell (EC) function. The present study examined whether T-cad deficiency increases vascular vulnerability in T2DM.
methodsVascular segments were isolated from WT or T-cad knockout mice. Endothelial function, total NO accumulation, and the expression of T-cad related proteins were determined.
resultsAch and acidified NaNO2 induced similar vasorelaxation in WT groups. T-cad KO mice exhibited normal response to acidified NaNO2, but manifested markedly reduced response to Ach. NO accumulation was also decreased in T-cad KO group. T-cad expression was reduced in WT mice fed 8 weeks of high fat diet (HFD). Furthermore, exacerbated reduction of vasorelaxation was observed in T-cad KO mice fed 8 weeks of HFD.
conclusionsIn the current study, we provide the first in vivo evidence that T-cadherin deficiency causes endothelial dysfunction in T2DM vascular segments, suggesting the involvement of T-cad deficiency in T2DM pathogenesis.
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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.