Coradduzza Donatella, Congiargiu Antonella, Chen Zhichao, Zinellu Angelo, Carru Ciriaco, Medici Serenella
Department of Biomedical Sciences, University of Sassari, 07100 Sassari, Italy.
Control Quality Unit, Azienda-Ospedaliera Universitaria (AOU), 07100 Sassari, Italy.
Int J Mol Sci. 2023 Feb 11;24(4):3658. doi: 10.3390/ijms24043658.
Senescence is a cellular aging process in all multicellular organisms. It is characterized by a decay in cellular functions and proliferation, resulting in increased cellular damage and death. This condition plays an essential role in the aging process and significantly contributes to the development of age-related complications. On the other hand, ferroptosis is a systemic cell death pathway characterized by excessive iron accumulation followed by the generation of reactive oxygen species (ROS). Oxidative stress is a common trigger of this condition and may be induced by various factors such as toxins, drugs, and inflammation. Ferroptosis is linked to numerous disorders, including cardiovascular disease, neurodegeneration, and cancer. Senescence is believed to contribute to the decay in tissue and organ functions occurring with aging. It has also been linked to the development of age-related pathologies, such as cardiovascular diseases, diabetes, and cancer. In particular, senescent cells have been shown to produce inflammatory cytokines and other pro-inflammatory molecules that can contribute to these conditions. In turn, ferroptosis has been linked to the development of various health disorders, including neurodegeneration, cardiovascular disease, and cancer. Ferroptosis is known to play a role in the development of these pathologies by promoting the death of damaged or diseased cells and contributing to the inflammation often associated. Both senescence and ferroptosis are complex pathways that are still not fully understood. Further research is needed to thoroughly investigate the role of these processes in aging and disease, and to identify potential interventions to target such processes in order to prevent or treat age-related conditions. This systematic review aims to assess the potential mechanisms underlying the link connecting senescence, ferroptosis, aging, and disease, and whether they can be exploited to block or limit the decay of the physiological functions in elderly people for a healthy longevity.
衰老 是所有多细胞生物中的一种细胞老化过程。其特征是细胞功能和增殖衰退,导致细胞损伤和死亡增加。这种状况在衰老过程中起着至关重要的作用,并显著促进与年龄相关并发症的发展。另一方面,铁死亡是一种全身性细胞死亡途径,其特征是铁过度积累,随后产生活性氧(ROS)。氧化应激是这种状况的常见触发因素,可能由毒素、药物和炎症等各种因素诱导。铁死亡与多种疾病有关,包括心血管疾病、神经退行性变和癌症。衰老被认为会导致随着年龄增长而出现的组织和器官功能衰退。它还与心血管疾病、糖尿病和癌症等与年龄相关的病理状况的发展有关。特别是,衰老细胞已被证明会产生炎症细胞因子和其他促炎分子,这些分子可能导致这些状况。反过来,铁死亡与包括神经退行性变、心血管疾病和癌症在内的各种健康疾病的发展有关。已知铁死亡通过促进受损或患病细胞的死亡并导致通常与之相关的炎症,在这些病理状况的发展中发挥作用。衰老和铁死亡都是复杂的途径,目前仍未完全了解。需要进一步研究以彻底调查这些过程在衰老和疾病中的作用,并确定针对这些过程的潜在干预措施,以预防或治疗与年龄相关的状况。本系统综述旨在评估衰老、铁死亡、衰老和疾病之间联系的潜在机制,以及它们是否可以被利用来阻止或限制老年人生理功能的衰退,以实现健康长寿。