Key result
Taurine transporter knockout in mice drives 14-fold greater interstitial cardiac fibrosis and pro-fibrotic gene expression.
Why the study?
The involvement of cardiac fibrosis in aging-dependent cardiac dysfunction caused by taurine depletion in TauT-knockout mice was unclear.
Taurine depletion predisposes the heart to a profibrotic gene expression pattern, leading to aging-related cardiac fibrosis in mice.
Taurine depletion may promote age-related cardiac fibrosis; hypothesis-generating for human trials and should not yet change practice.
Dietary taurine deficiency results in dilated cardiomyopathy in cats while in mice taurine deficiency produced by knocking out the taurine transporter (TauT) gene leads to a reduction in cardiac function with advancing age. The present study elucidated the involvement of cardiac fibrosis in the aging-dependent cardiac disorder of the TauT-knockout (TauTKO) mouse. Old (18-24-month-old) TauTKO mice, but not young (3-5-month-old) mice, exhibit cardiac fibrosis. Transcriptome microarray analysis revealed an increase in pro-fibrotic genes, such as S100A4, ACTA2 and CTGF, in both young and old TauTKO hearts. Based on transcriptome-pathway analysis the genes involved in "organization of extracellular matrix," such as LGALS3, are enriched in old TauTKO hearts compared to old wild-type hearts, suggesting the contribution of these genes to fibrosis. In conclusion, taurine depletion predisposes the heart to fibrosis, which leads to cardiac fibrosis upon aging.
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Ito et al. (2018) studied Aging-related cardiac fibrosis. Taurine depletion (TauT knockout) vs. Wild-type mice was evaluated on Interstitial cardiac fibrosis (14-fold greater, p=<0.05). Old taurine transporter knockout mice exhibited a 14-fold greater interstitial cardiac fibrosis compared to old wild-type mice, alongside increased pro-fibrotic gene expression.
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