目的:血红素加氧酶-1(HO-1)是血红素代谢的关键酶,促进血红素分解成胆绿素,一氧化碳,免费的铁。以其强大的细胞保护特性而闻名,HO-1展示了显著的抗氧化剂,抗炎,和抗凋亡作用。在这次审查中,作者旨在探讨HO-1对心脏衰老的深远影响及其在心肌梗死(MI)中的潜在意义.
结果:最近的研究揭示了HO-1在细胞衰老中的复杂作用,以不可逆的生长停滞和功能衰退为特征。值得注意的是,心脏衰老已成为各种心血管疾病发展的关键因素,包括MI。值得注意的是,心脏衰老已成为各种心血管疾病发展的重要因素,包括心肌梗死(MI)。衰老细胞的积累,跨越血管内皮细胞,血管平滑肌细胞,心肌细胞,和祖细胞,对心血管疾病如血管老化构成重大风险,动脉粥样硬化,心肌梗塞,和心室重构。抑制心肌细胞衰老不仅减少衰老相关的炎症,而且影响其他心肌谱系。暗示病理性重塑中更广泛的传播机制。HO-1已被证明可以改善心脏功能并减轻缺血性损伤和衰老引起的心肌细胞衰老。此外,已发现HO-1诱导可缓解H2O2诱导的心肌细胞衰老。随着我们对抗增殖的理解的增长,抗血管生成,抗衰老,和HO-1的血管效应,我们看到了利用个体对心脏衰老的易感性和心肌梗死之间的潜在联系的潜力。
结论:这篇综述研究了上调HO-1的策略,包括基因靶向和药物,作为潜在的治疗方法。通过从不同的实验模型和临床研究中综合令人信服的证据,这项研究阐明了靶向HO-1作为减轻心脏衰老和改善心肌梗死预后的创新策略的治疗潜力。强调需要在这一领域进一步研究。
OBJECTIVE: Heme oxygenase-1 (HO-1) is a crucial enzyme in heme metabolism, facilitating the breakdown of heme into biliverdin, carbon monoxide, and free iron. Renowned for its potent cytoprotective properties, HO-1 showcases notable antioxidant, anti-inflammatory, and anti-apoptotic effects. In this
review, the authors aim to explore the profound impact of HO-1 on cardiac senescence and its potential implications in myocardial infarction (MI).
RESULTS: Recent research has unveiled the intricate role of HO-1 in cellular senescence, characterized by irreversible growth arrest and functional decline. Notably, cardiac senescence has emerged as a pivotal factor in the development of various cardiovascular conditions, including MI. Notably, cardiac senescence has emerged as an important factor in the development of various cardiovascular conditions, including myocardial infarction (MI). The accumulation of senescent cells, spanning vascular endothelial cells, vascular smooth muscle cells, cardiomyocytes, and progenitor cells, poses a significant risk for cardiovascular diseases such as vascular aging, atherosclerosis, myocardial infarction, and ventricular remodeling. Inhibition of cardiomyocyte senescence not only reduces senescence-associated inflammation but also impacts other myocardial lineages, hinting at a broader mechanism of propagation in pathological remodeling. HO-1 has been shown to improve heart function and mitigate cardiomyocyte senescence induced by ischemic injury and aging. Furthermore, HO-1 induction has been found to alleviate H2O2-induced cardiomyocyte senescence. As we grow in our understanding of antiproliferative, antiangiogenic, anti-aging, and vascular effects of HO-1, we see the potential to exploit potential links between individual susceptibility to cardiac senescence and myocardial infarction.
CONCLUSIONS: This
review investigates strategies for upregulating HO-1, including gene targeting and pharmacological agents, as potential therapeutic approaches. By synthesizing compelling evidence from diverse experimental models and clinical investigations, this study elucidates the therapeutic potential of targeting HO-1 as an innovative strategy to mitigate cardiac senescence and improve outcomes in myocardial infarction, emphasizing the need for further research in this field.