Ferroptosis and Senescence: A Systematic Review.
Donatella CoradduzzaAntonella CongiargiuZhichao ChenAngelo ZinelluCiriaco CarruSerenella MediciPublished in: International journal of molecular sciences (2023)
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.
Keyphrases
- cell death
- cell cycle arrest
- cardiovascular disease
- oxidative stress
- dna damage
- induced apoptosis
- systematic review
- papillary thyroid
- endothelial cells
- reactive oxygen species
- type diabetes
- squamous cell
- signaling pathway
- healthcare
- public health
- squamous cell carcinoma
- physical activity
- cardiovascular events
- coronary artery disease
- randomized controlled trial
- mental health
- metabolic syndrome
- weight gain
- ischemia reperfusion injury
- childhood cancer
- climate change
- risk assessment
- body mass index
- lymph node metastasis
- sensitive detection
- cell proliferation
- insulin resistance
- health information
- single molecule
- multidrug resistant