Scholarlink

<p>Prolonged social isolation (SI) and negative emotion are associated with an increased risk of cardiovascular diseases (CVDs). However, it remains elusive whether SI and emotional states affect the pathological process of myocardial infarction (MI). In this study, SI models with different duration and MI model were co-established in mice. Anxiety and depression were assessed by a series of behavioral tests including open field test, elevated plus maze test, novelty-suppressed feeding test, tail suspension test and forced swim test. Cardiac function, heart infarct size and fibrosis were assessed by echocardiography, TTC staining, and Masson staining. The activity of neurons across the whole brain, as well as the hypothalamic-pituitary-adrenal (HPA) axis, was also investigated. Long-term SI induced anxiety and depression-like behaviors and aggravated cardiac injury and inflammatory response in MI mice, while short-term SI induced anxiety-like behavior but not depression-like behavior and had no significant effects on cardiac injury. Long-term SI altered the activity of several brain regions related to emotional, reward, autonomic and neuroendocrine regulation in MI mice. Furthermore, serum corticosterone levels were altered, indicating the potential involvement of HPA axis. These findings reveal that long-term SI exacerbated cardiac dysfunction and cardiac injury after MI. The underlying mechanisms involved in this process may include negative mood, dysregulation of the reward system, autonomic nervous system modulation, and HPA axis activation. These findings will contribute to our better understanding of heart-brain connections.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Long-term social isolation during adolescence exacerbated cardiac dysfunction after myocardial infarction

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月20日

查看全文
  • Yuan Yao,
  • Anhui Wang,
  • Chang Di,
  • Dan Guo,
  • Shiya Zhang,
  • Runzhe Zong,
  • Rong Qi,
  • Ying Han

摘要

Prolonged social isolation (SI) and negative emotion are associated with an increased risk of cardiovascular diseases (CVDs). However, it remains elusive whether SI and emotional states affect the pathological process of myocardial infarction (MI). In this study, SI models with different duration and MI model were co-established in mice. Anxiety and depression were assessed by a series of behavioral tests including open field test, elevated plus maze test, novelty-suppressed feeding test, tail suspension test and forced swim test. Cardiac function, heart infarct size and fibrosis were assessed by echocardiography, TTC staining, and Masson staining. The activity of neurons across the whole brain, as well as the hypothalamic-pituitary-adrenal (HPA) axis, was also investigated. Long-term SI induced anxiety and depression-like behaviors and aggravated cardiac injury and inflammatory response in MI mice, while short-term SI induced anxiety-like behavior but not depression-like behavior and had no significant effects on cardiac injury. Long-term SI altered the activity of several brain regions related to emotional, reward, autonomic and neuroendocrine regulation in MI mice. Furthermore, serum corticosterone levels were altered, indicating the potential involvement of HPA axis. These findings reveal that long-term SI exacerbated cardiac dysfunction and cardiac injury after MI. The underlying mechanisms involved in this process may include negative mood, dysregulation of the reward system, autonomic nervous system modulation, and HPA axis activation. These findings will contribute to our better understanding of heart-brain connections.