Aging At The Crossroads Of Cuproptosis And Ferroptosis: From Molecular Pathways To Age-Related Pathologies And Therapeutic Perspectives
As we age, our bodies experience a gradual decline in function and become more susceptible to various illnesses, including conditions like Alzheimer’s, heart disease, and cancer. This process is often accompanied by chronic, low-grade inflammation, problems with our cells’ energy-producing centers (mitochondria), and an increase in harmful molecules called reactive oxygen species, leading to what scientists call oxidative stress.
Recent research sheds light on two crucial forms of regulated cell death, known as ferroptosis and cuproptosis, that play a significant role in these age-related changes. Ferroptosis is a type of cell death that depends on iron and involves the damaging of fats within cells, a process called lipid peroxidation, often due to issues with an important protective enzyme called glutathione peroxidase 4 (GPX4). Cuproptosis, on the other hand, is a copper-dependent process linked to stress in how certain proteins are modified, a process known as protein lipoylation.
These two cell death pathways are not isolated but are deeply interconnected within a broader network involving metals, cellular energy, and the balance of oxidation and reduction reactions in the body. When the balance of copper or iron is disrupted, or when GPX4 function is impaired, or mitochondria are compromised, it can make cells more vulnerable. This increased vulnerability can worsen oxidative damage, immune system dysfunction, and tissue degeneration, ultimately accelerating aging and inflammation.
Understanding these intricate connections offers new avenues for addressing age-related diseases. By targeting these specific cell death pathways through interventions like dietary adjustments, medications, and lifestyle changes, there is potential to develop new strategies to promote healthier aging and combat age-related pathologies.
Source: link to paper