Volume 2,Issue 9
Fall 2024
自噬在心肌肥厚中的研究进展
自噬是心肌细胞肥大的重要分子机制之一。自噬过程涉及多个层面,包括自噬体的形成、成熟和降解,这些过程在心肌肥厚的发展中起着关键作用。研究显示,自噬在生理性心肌肥厚和病理性心肌肥厚中的作用有所不同。生理性心肌肥厚中,自噬被适度激活,通过清除受损细胞器和错误折叠蛋白,维持心肌细胞稳态。在病理性心肌肥厚中具有双重性:一方面,自噬可能作为一种代偿机制,在心肌肥厚早期发挥保护作用;另一方面,随着疾病进展,自噬的降低可能导致细胞质组件降解减少,从而促进肥厚。过度的自噬可能破坏自噬流的平衡,损伤必要的蛋白质与细胞器,引起细胞凋亡,并推动疾病向失代偿性心衰进展。
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