心力衰竭降低了脂肪细胞原始体,对成熟脂肪细胞的分化能力受损
Yusuke Takeda1, Oto Inoue1,2, Ayano Nomura1
1Department of Cardiovascular Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
概括
心力衰竭 (HF) 降低了脂肪细胞原生细胞 (APC) 的数量和功能,导致脂肪组织损失和恶化的HF结果. 准APC可能为HF患者的缓冲症提供新的治疗策略.
科学领域:
- 心血管生物学 心血管生物学
- 脂肪组织生物学 脂肪组织生物学
- 疾病的细胞机制.
背景情况:
- 通过脂肪组织缩标志着心脏缓解症,是心力衰竭 (HF) 的严重并发症.
- 脂肪组织功能障碍可以加剧HF,突出其代谢和内分泌心脏保护作用.
- 脂肪细胞原生细胞 (APC) 对于维持脂肪组织平衡至关重要,但它们在HF中的作用尚不清楚.
研究的目的:
- 研究HF对小鼠皮下脂肪细胞原生细胞 (APC) 的数量和功能的影响.
- 阐明HF影响APC的机制,包括增殖,亡和分化.
- 探索交感神经活动在高频诱导的APC功能障碍中的作用.
主要方法:
- 在小鼠中使用横向大动脉收缩诱导心力衰竭 (HF).
- 在皮下脂肪组织中对Lin-CD24+ APCs的量化和表征.
- 在体外测试以评估APC增殖,细胞亡和脂肪生成差异化.
- 脂肪组织脱皮 (ATD) 来评估交感神经的作用.
主要成果:
- 肝炎显著降低了APC数量,并增加了细胞亡,导致脂质营养不良.
- 在试验室中,HF损害了APC增殖和诱导衰老.
- 增加的交感神经活动部分调解了HF诱导的APC损失和衰老.
- 高频率和增加的同情活动降低了APC的基分化能力.
结论:
- 心力衰竭诱导APC损失和衰老,部分是通过增加交感神经活动.
- 损坏的APC功能和减少的脂肪组织质量有助于HF的恶化.
- 在心力衰竭中,APCs代表了一种新的治疗点,用于控制缓解症和改善心力衰竭的结果.
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