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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Related Experiment Video

Updated: May 27, 2025

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
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TRPV4 Promotes Vascular Calcification by Directly Associating With and Activating β-Catenin.

Menglu Yuan1, Qi Li1, Zhiwei Wang1

  • 1Department of Basic Medicine, Wuxi School of Medicine, Jiangnan University, China. MOE Medical Basic Research Innovation Center for Gut Microbiota and Chronic Diseases, Wuxi School of Medicine, Jiangnan University, China.

Arteriosclerosis, Thrombosis, and Vascular Biology
|February 20, 2025
PubMed
Summary
This summary is machine-generated.

Transient receptor potential channel V4 (TRPV4) drives vascular calcification by activating β-catenin. Blocking this TRPV4/β-catenin interaction with hesperidin offers a potential therapeutic strategy for preventing vascular calcification.

Keywords:
TRPV cation channelscateninshesperidinmuscle, smooth, vascularvascular calcification

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Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Nephrology

Background:

  • Vascular calcification is a major contributor to cardiovascular disease in patients with chronic kidney disease, diabetes, and atherosclerosis.
  • Current therapeutic strategies for vascular calcification are limited.
  • The role of TRPV4 (transient receptor potential channel V4) in vascular calcification remains unclear.

Purpose of the Study:

  • To investigate the role and mechanism of TRPV4 in vascular calcification.
  • To explore potential therapeutic strategies targeting TRPV4.

Main Methods:

  • In vitro and in vivo studies of TRPV4 effects on vascular calcification.
  • TRPV4 interactome assessment and molecular docking.
  • Analysis of osteochondrogenic markers and signaling pathways.

Main Results:

  • TRPV4 was upregulated in calcified vascular smooth muscle cells and aortas.
  • TRPV4 overexpression exacerbated calcification, while deficiency inhibited it.
  • TRPV4 interacted with β-catenin, activating the β-catenin/TCF pathway via Ca2+/ASK1/p38 signaling.
  • Hesperidin disrupted TRPV4/β-catenin interaction, preventing calcification.

Conclusions:

  • TRPV4 is identified as a pathogenic factor in vascular calcification.
  • TRPV4 directly associates with and activates β-catenin.
  • Blocking the TRPV4/β-catenin interaction with hesperidin is a promising precision strategy to inhibit vascular calcification progression.