人类患者和动物模型中心力衰竭引起的骨肌肉组织学变化:范围审查
Akinori Kaneguchi1, Naoyoshi Sakitani2, Takuya Umehara1
1Department of Rehabilitation, Faculty of Rehabilitation, Hiroshima International University, Kurose-Gakuendai 555-36, Higashi-Hiroshima, Hiroshima, 739-2695, Japan.
Acta histochemica
|October 23, 2024
概括
心力衰竭 (HF) 导致骨肌肉发生变化,包括纤维缩和亡增加. 这些组织学变化可能解释HF患者的肌肉衰弱和疲劳,动物模型显示了类似的趋势.
科学领域:
- 心血管科学 心血管科学
- 肌肉生理学 肌肉生理学
- 组织病理学 组织病理学
背景情况:
- 心力衰竭 (HF) 与显著的骨肌肉功能障碍有关.
- 了解骨肌肉的组织学变化对于管理HF并发症至关重要.
研究的目的:
- 在心力衰竭 (HF) 之后,对骨肌肉的组织学变化进行表征.
- 识别有关HF诱导的骨肌肉变化的知识差距.
主要方法:
- 2024年4月3日进行的系统文献搜索.
- 包括对HF患者和动物模型骨肌肉组织学分析的研究.
- 由两个独立作者进行的选和数据提取.
主要成果:
- 选择了118篇论文 (33篇人类,85篇动物研究).
- 观察到的趋势:纤维过渡缓慢到快速,纤维大小减少,毛细血管与纤维的比率,以及线粒体含量/活性.
- 观察到亡的增加,可能会导致肌肉疲劳和软弱.
结论:
- HF诱导了骨肌肉中一致的组织学变化,主要反映在动物模型中.
- 需要进一步的研究来确定这些变化是否发生在上肢肌肉中.
- 巩固的知识有助于HF患者的康复和未来的研究.
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