Dietary selenium deficiency drives sex-specific circadian disturbance through redox imbalance and causes early systolic dysfunction in mice
- 1University Medical Center Groningen
Abstract
Background: Selenium is a vital trace element involved in antioxidant defence and cardiovascular health. Although selenium deficiency is implicated in cardiomyopathies, its early cardiac effects and underlying mechanisms remain poorly defined. Methods: C57BL6/Njr mice were fed either a selenium deficient or control diet for 12 weeks. Systemic selenium status, cardiac function by echocardiography, left ventricular (LV) transcriptomic profiles, redox balance, and circadian pathway markers were assessed, including sex-specific analyses. Results: Selenium deficiency reduced plasma selenium levels without inducing overt cardiac hypertrophy or fibrosis. Echocardiography showed preserved ejection fraction and fractional shortening but reduced global longitudinal strain, indicating early systolic dysfunction. Cardiac stress markers were increased predominantly in male mice. Left ventricular RNA sequencing revealed enrichment of pathways related to cardiac remodelling, redox regulation, mitochondrial function, and circadian rhythm. Additional protein and metabolic analyses supported sex-specific redox circadian alterations, with males showing a more pronounced stress response profile. Conclusions: Dietary selenium deficiency induces early myocardial dysfunction and molecular remodelling before overt cardiac failure. These changes are associated with redox and circadian pathway disruption and show sex specific features, suggesting that selenium contributes to cardiac homeostasis through sex dependent redox circadian regulation.
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BibTeX
@misc{guo2026dietary,
title = {{Dietary selenium deficiency drives sex-specific circadian disturbance through redox imbalance and causes early systolic dysfunction in mice}},
author = {X. Guo and F. Lambregtse and L. Geerlings and J. Zhu and S. N. Zijlstra and A. M. Feringa and E. M. Schouten and H. H. Sillje and L. Schomburg and P. van der Meer and N. Bomer},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.28.754959},
url = {https://www.biorxiv.org/content/10.64898/2026.09.28.754959v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Dietary selenium deficiency drives sex-specific circadian disturbance through redox imbalance and causes early systolic dysfunction in mice
AU - X. Guo
AU - F. Lambregtse
AU - L. Geerlings
AU - J. Zhu
AU - S. N. Zijlstra
AU - A. M. Feringa
AU - E. M. Schouten
AU - H. H. Sillje
AU - L. Schomburg
AU - P. van der Meer
AU - N. Bomer
PY - 2026
DA - 2026/09/28
PB - bioRxiv
DO - 10.64898/2026.09.28.754959
UR - https://www.biorxiv.org/content/10.64898/2026.09.28.754959v1
AB - Background: Selenium is a vital trace element involved in antioxidant defence and cardiovascular health. Although selenium deficiency is implicated in cardiomyopathies, its early cardiac effects and underlying mechanisms remain poorly defined. Methods: C57BL6/Njr mice were fed either a selenium deficient or control diet for 12 weeks. Systemic selenium status, cardiac function by echocardiography, left ventricular (LV) transcriptomic profiles, redox balance, and circadian pathway markers were assessed, including sex-specific analyses. Results: Selenium deficiency reduced plasma selenium levels without inducing overt cardiac hypertrophy or fibrosis. Echocardiography showed preserved ejection fraction and fractional shortening but reduced global longitudinal strain, indicating early systolic dysfunction. Cardiac stress markers were increased predominantly in male mice. Left ventricular RNA sequencing revealed enrichment of pathways related to cardiac remodelling, redox regulation, mitochondrial function, and circadian rhythm. Additional protein and metabolic analyses supported sex-specific redox circadian alterations, with males showing a more pronounced stress response profile. Conclusions: Dietary selenium deficiency induces early myocardial dysfunction and molecular remodelling before overt cardiac failure. These changes are associated with redox and circadian pathway disruption and show sex specific features, suggesting that selenium contributes to cardiac homeostasis through sex dependent redox circadian regulation.
ER -