Thyroid hormone receptor blockade by amiodarone disrupts angiogenesis via <scp>VEGFα</scp>, <scp>WNT7A</scp>, <scp>BMP</scp>, and <scp>PI3K</scp>/<scp>AKT</scp> pathways in chick embryo vascular development

Our findings underscore the essential role of thyroid hormone signaling in embryonic angiogenesis. Disruption of TR activation by amiodarone significantly impairs vascular formation through coordinated suppression of Vascular endothelial growth factor alpha (VEGFα), WNT7A, bone morphogenetic proteins, and PI3K/AKT pathways. These insights enhance our understanding of TH-related developmental disorders and may guide therapeutic strategies for managing vascular dysfunctions associated with impaired thyroid signaling.

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Publication Details

Journal
Developmental Dynamics
Published
2025-09-13
DOI
https://doi.org/10.1002/dvdy.70076
Citations
1
Primary Topic
Congenital heart defects research
Type
article
Field-Weighted Citation Impact
0.81
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article

Thyroid hormone receptor blockade by amiodarone disrupts angiogenesis via VEGFα, WNT7A, BMP, and PI3K/AKT pathways in chick embryo vascular development

Juhi Vaishnav, Suresh Balakrishnan
1 citations
Developmental Dynamics
Congenital heart defects research
0.81
article

Thyroid hormone receptor blockade by amiodarone disrupts angiogenesis via VEGFα, WNT7A, BMP, and PI3K/AKT pathways in chick embryo vascular development

Juhi Vaishnav, Suresh Balakrishnan
article en
1 citations

Abstract

Our findings underscore the essential role of thyroid hormone signaling in embryonic angiogenesis. Disruption of TR activation by amiodarone significantly impairs vascular formation through coordinated suppression of Vascular endothelial growth factor alpha (VEGFα), WNT7A, bone morphogenetic proteins, and PI3K/AKT pathways. These insights enhance our understanding of TH-related developmental disorders and may guide therapeutic strategies for managing vascular dysfunctions associated with impaired thyroid signaling.

Developmental Dynamics
Maharaja Sayajirao University of Baroda (IN)
Openalex Percentile: Top 24%
Congenital heart defects research
0.81
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