Ferroptosis and Senescence: A Systematic Review

Abstract

Background: Senescence is a cellular ageing process in all multicellular organisms. It is characterized by a decline in cellular functions and proliferation, resulting in increased cellular damage and death. This condition plays an essential role in the ageing process and significantly contributes to the development of age-related complications. On the other hand, ferroptosis is a systemic cell death 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 illnesses, including cardiovascular disease, neurodegeneration, and cancer. Relevance of these conditions to ageing and disease: Senescence is believed to contribute to the decline in tissue and organ function that occurs with ageing. 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. On the other hand, ferroptosis has been linked to the development of various health disorders, including neurodegeneration, cardiovascular disease, and cancer [1]. It is known to play a role in developing these diseases by promoting the death of damaged or diseased cells and contributing to the inflammation often associated with them. Both senescence and ferroptosis are complex processes that are still not fully understood. Further research is needed to thoroughly understand the role of these processes in ageing and disease, and to identify potential interventions to target these processes to prevent or treat age-related conditions. Objectives: This systematic review aims to assess the potential mechanisms underlying the link connecting senescence, ferroptosis, ageing, and disease.

Iron chelators as a therapeutic option for Alzheimer’s disease—A mini-review

“…Ferroptosis, a type of programmed cell death first described in 2012 (Dixon et al, 2012), involves lipid peroxidation generated by the iron overload, leading to cell swelling, mitochondrial dysfunction, nuclear chromatin condensation, and, finally, cellular membrane rupture (Han et al, 2020). Various studies have shown a correlation between the accumulation of iron in the brain which means increased ferroptosis and aging (Coradduzza et al, 2023), cerebrovascular diseases (Liu et al, 2022), and neurodegenerative diseases (including AD) (Ma et al, 2022). However, the exact molecular mechanisms of iron-induced neurodegeneration remain incompletely known.…”

Ferroptosis and the ubiquitin-proteasome system: exploring treatment targets in cancer

“…The primary goal of cancer treatment research has been to eliminate malignant cells while protecting healthy cells (Cassetta and Pollard, 2023). To prevent the uncontrolled growth of cancer cells and other abnormal tissues, the body relies on a process known as "regulated cell death" (RCD) to keep things in check (Coradduzza et al, 2023;Huang et al, 2023). Apoptosis, paraptosis, necroptosis, and ferroptosis are among the distinct modes of RCD that have been characterized so far (Tong et al, 2022).…”

Editorial: Targeting oxidative stress in cancer: what is new in the prevention, diagnostic, treatment and prognostic strategies?

“…Oxidative stress plays an essential role in cancer development and progression since high levels of reactive oxygen species (ROS) can trigger damage to biomolecules, promoting carcinogenesis (Cheung and Vousden, 2022). On the other hand, this metabolic imbalance may result in cell death by different mechanisms, becoming the induction of oxidative stress a potential strategy in anticancer therapy (Luo et al, 2022;Coradduzza et al, 2023).…”