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<p>Here we systematically compared the cardiovascular effects of continuous light (LL) and reversed 48-hour light-dark cycle (LD-DL) exposure in Sprague-Dawley rats over 20 weeks. Both disrupted light conditions were associated with significant cardiovascular dysfunction, including elevated blood pressure and increased heart rate, along with myocardial hypertrophy, cardiac enlargement, collagen fibrosis, and apoptosis. Notably, the LD-DL group exhibited more pronounced oxidative stress (elevated ROS, downregulated Nrf2) and inflammatory responses (enhanced inflammatory cell infiltration, upregulated IL-6 and IL-1β), whereas the LL group showed more pronounced cardiac structural remodeling despite moderate inflammation. Both paradigms were accompanied by suppressed melatonin levels and altered clock gene expression. These findings suggest that distinct light disruption patterns may be associated with cardiovascular injury through different mechanisms—LL predominantly characterized by hemodynamic parameters and structural remodeling, LD-DL preferentially linked to oxidative-inflammatory responses—highlighting the need for paradigm-specific therapeutic strategies.</p>

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Disrupted light exposure is associated with cardiac remodeling involving clock gene alterations and oxidative–inflammatory responses in rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月1日

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  • Xueling Li,
  • Qin Zhu,
  • Hongyu Chen,
  • Xiaodi Hu,
  • Yang Zhang,
  • Likai Han,
  • Qinyang Jin

摘要

Here we systematically compared the cardiovascular effects of continuous light (LL) and reversed 48-hour light-dark cycle (LD-DL) exposure in Sprague-Dawley rats over 20 weeks. Both disrupted light conditions were associated with significant cardiovascular dysfunction, including elevated blood pressure and increased heart rate, along with myocardial hypertrophy, cardiac enlargement, collagen fibrosis, and apoptosis. Notably, the LD-DL group exhibited more pronounced oxidative stress (elevated ROS, downregulated Nrf2) and inflammatory responses (enhanced inflammatory cell infiltration, upregulated IL-6 and IL-1β), whereas the LL group showed more pronounced cardiac structural remodeling despite moderate inflammation. Both paradigms were accompanied by suppressed melatonin levels and altered clock gene expression. These findings suggest that distinct light disruption patterns may be associated with cardiovascular injury through different mechanisms—LL predominantly characterized by hemodynamic parameters and structural remodeling, LD-DL preferentially linked to oxidative-inflammatory responses—highlighting the need for paradigm-specific therapeutic strategies.