Enhancing Near-Room-Temperature Thermoelectric Performance of n-Type Mg(3)(Sb, Bi)(2)-Based Materials via ZrB(2) Heterointerface Engineering.

Various types of cell death, as fundamental physiological processes, play a vital role throughout an organism’s life cycle, from initial embryonic development to the maintenance of homeostasis and ultimately aging and death (Bertheloot et al., 2021). In addition to their physiological roles, cell death processes can also have pathological implications, as abnormal cell death often leads to disease (Yan et al., 2021). Cell death can be categorized into two main types: accidental cell death and regulated cell death (RCD). Accidental cell death is primarily an uncontrolled process that occurs in response to external stimuli or injuries, whereas RCD is a type of cell death that is regulated by biological factors and plays a more extensive role in the life cycle of organisms (Tong et al., 2022). Ferroptosis is a specific mode of RCD characterized by disruptions in iron metabolism and the accumulation of lipid peroxides. Numerous studies have confirmed that ferroptosis is crucial for sustaining human health and is involved in the occurrence and progression of various diseases (Jiang et al., 2021; Sun et al., 2023). Neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS), have an incidence that is positively correlated with aging. Currently, there is no cure for these diseases, which places a heavy burden on society and patients’ families. It is estimated that by 2050, neurodegenerative diseases will affect approximately 150 million people worldwide, resulting in economic burdens of up to 10 trillion US dollars (Temple, 2023). One of the main causes of neurodegenerative diseases is the premature death of neural cells that are essential for maintaining the function of the nervous system (Yuan and Ofengeim, 2024). The abnormal activation of RCD in neural cells is a characteristic pathological change observed in these diseases (Moujalled et al., 2021). Furthermore, numerous studies have confirmed that iron deposition (Ayton et al., 2020; Ma et al., 2021) and lipid peroxidation (Ansari and Scheff, 2010; Hatami et al., 2018) are significant risk factors for neurodegenerative diseases. Ferroptosis inhibitors appear to delay disease progression (Yan et al., 2021). It is well known that aging-related iron deposition and lipid peroxidation also contribute to ferroptosis (Coradduzza et al., 2023). Additionally, we have previously elucidated that ferroptosis is a significant mode of cell death following spinal cord injury (Song et al., 2024), and inhibiting ferroptosis shows promise for reversing neurological dysfunction (Song et al., 2023a). Therefore, ferroptosis is likely to be a key contributor to the pathogenesis of neurodegenerative diseases and is expected to emerge as a new therapeutic target. In this review, we summarize the latest advancements in research regarding the mechanisms and pathways of ferroptosis, its relationship with aging, its association with neurodegenerative diseases, and potential treatments (). Based on the findings of relevant studies, we conclude that the mechanism of ferroptosis is complex and regulated by multiple factors. Numerous studies have confirmed that ferroptosis can contribute to the pathogenesis of neurodegenerative diseases through various mechanisms, mediating neuronal cell death. Additionally, ferroptosis can trigger the onset of these diseases and accelerate their progression.