T-Cadherin Deficiency Is Associated with Increased Blood Pressure after Physical Activity
Popov VS., Brodsky IB., Balatskaya MN., Balatskiy AV., Ozhimalov ID., Kulebyakina MA.
Animal Study, published in Int J Mol Sci (2023) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Int J Mol Sci (2023)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 37762507
- PMCID
- PMC10531645
- DOI
- 10.3390/ijms241814204
- Citations
- 8
Abstract (original English)
T-cadherin is a regulator of blood vessel remodeling and angiogenesis, involved in adiponectin-mediated protective effects in the cardiovascular system and in skeletal muscles. GWAS study has previously demonstrated a SNP in the Cdh13 gene to be associated with hypertension. However, the role of T-cadherin in regulating blood pressure has not been experimentally elucidated. Herein, we generated Cdh13 ∆Exon3 mice lacking exon 3 in the Cdh13 gene and described their phenotype. Cdh13 ∆Exon3 mice exhibited normal gross morphology, life expectancy, and breeding capacity. Meanwhile, their body weight was considerably lower than of WT mice. When running on a treadmill, the time spent running and the distance covered by Cdh13 ∆Exon3 mice was similar to that of WT. The resting blood pressure in Cdh13 ∆Exon3 mice was slightly higher than in WT, however, upon intensive physical training their systolic blood pressure was significantly elevated. While adiponectin content in the myocardium of Cdh13 ∆Exon3 and WT mice was within the same range, adiponectin plasma level was 4.37-fold higher in Cdh13 ∆Exon3 mice. Moreover, intensive physical training augmented the AMPK phosphorylation in the skeletal muscles and myocardium of Cdh13 ∆Exon3 mice as compared to WT. Our data highlight a critically important role of T-cadherin in regulation of blood pressure and stamina in mice, and may shed light o
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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