【摘要】 慢性心力衰竭病理机制复杂，涉及心肌细胞凋亡、氧化应激等多环节，含锚蛋白重复序列-细胞因子信号抑制物盒蛋白家族10(Asb10)/热休克蛋白70(HSP70)轴失衡在其发生发展中起关键作用。Asb10作为E3泛素连接酶介导HSP70降解，削弱后者抗凋亡、抗氧化及线粒体保护功能。目前，靶向该轴的小分子抑制剂、基因治疗及生物制剂等策略已展现出一定潜力，与传统药物，如血管紧张素转化酶抑制剂（ACEI）或β受体阻滞剂联合使用可产生协同效应，但面临特异性不足、递送效率低等挑战。未来需聚焦精准调控、联合干预及时空动态治疗，推动慢性心力衰竭从对症向机制靶向治疗转化。更多还原

【Abstract】 The pathophysiological mechanisms of chronic heart failure are complex, involving multiple processes such as cardiomyocyte apoptosis and oxidative stress. The imbalance of the Ankyrin Repeat and SOCS Box Containing 10(Asb10)/Heat Shock Protein 70(HSP70) axis plays a key role in its development. Asb10,acting as an E3 ubiquitin ligase, mediates HSP70 degradation, thereby weakening its anti-apoptotic, antioxidant,and mitochondrial protective functions. Currently, strategies targeting this axis—including small molecule inhibitors, gene therapies, and biologics—have shown promising potential. When combined with conventional drugs like angiotensin-converting enzyme inhibitor(ACEI) and beta-blockers, these therapies can produce synergistic effects. However, challenges remain, including insufficient specificity and low delivery efficiency.Future research should focus on precise regulation and timely spatiotemporal dynamic interventions to advance chronic heart failure treatment from symptom-based approaches to mechanism-targeted therapies.更多还原