Age and age-related diseases are closely linked to inflammation and cytokine dysregulation. As people age, the immune system becomes less effective at controlling inflammation, leading to a pro-inflammatory state known as "inflamm-aging." This condition is associated with various age-related diseases, including atherosclerosis, diabetes, Alzheimer's disease, rheumatoid arthritis, and cancer. While inflammation is a normal part of the body's healing process, chronic or excessive inflammation can be harmful. Several molecular pathways, such as redox imbalance, senescent cells, and reduced autophagy, contribute to the pro-inflammatory environment in aging. The senescence-associated secretory phenotype (SASP) is a key factor in this process, as it promotes a self-perpetuating inflammatory cycle. The inflammasome, particularly the NLRP3 inflammasome, plays a critical role in initiating and maintaining inflammation. It is activated by various stress signals, including mitochondrial dysfunction, damaged cells, and harmful molecules. The NLRP3 inflammasome activates pro-inflammatory cytokines such as IL-1β and IL-18, which contribute to chronic inflammation. Inflammation can be resolved through specialized pro-resolving mediators (SPMs), which help to restore immune homeostasis. However, aging reduces the body's ability to resolve inflammation effectively, leading to persistent inflammation and disease. Pro-inflammatory cytokines such as IL-1 and IL-18 are key mediators of inflammation in aging and age-related diseases. Their dysregulation is associated with increased inflammation and disease progression. The IL-1 family of cytokines, including IL-1α, IL-1β, and IL-18, plays a central role in the inflammatory response. IL-1β is cleaved by caspase-1 to become active, while IL-1α is activated by calpain protease. These cytokines bind to their respective receptors, triggering inflammatory signaling pathways. Age-related changes in the expression and activity of these cytokines contribute to the pro-inflammatory state seen in aging. The balance between pro-inflammatory and anti-inflammatory cytokines is crucial for maintaining immune homeostasis. Dysregulation of this balance can lead to chronic inflammation and age-related diseases. Research into the molecular pathways underlying inflammation and resolution is essential for developing new therapies to improve aging and treat age-related diseases. Potential therapeutic strategies include targeting the inflammasome, enhancing autophagy, and using pharmacological mimetics of pro-resolving mediators. Lifestyle factors, such as diet and exercise, also play a role in modulating inflammation and aging. Understanding these mechanisms is key to developing effective interventions for age-related diseases.Age and age-related diseases are closely linked to inflammation and cytokine dysregulation. As people age, the immune system becomes less effective at controlling inflammation, leading to a pro-inflammatory state known as "inflamm-aging." This condition is associated with various age-related diseases, including atherosclerosis, diabetes, Alzheimer's disease, rheumatoid arthritis, and cancer. While inflammation is a normal part of the body's healing process, chronic or excessive inflammation can be harmful. Several molecular pathways, such as redox imbalance, senescent cells, and reduced autophagy, contribute to the pro-inflammatory environment in aging. The senescence-associated secretory phenotype (SASP) is a key factor in this process, as it promotes a self-perpetuating inflammatory cycle. The inflammasome, particularly the NLRP3 inflammasome, plays a critical role in initiating and maintaining inflammation. It is activated by various stress signals, including mitochondrial dysfunction, damaged cells, and harmful molecules. The NLRP3 inflammasome activates pro-inflammatory cytokines such as IL-1β and IL-18, which contribute to chronic inflammation. Inflammation can be resolved through specialized pro-resolving mediators (SPMs), which help to restore immune homeostasis. However, aging reduces the body's ability to resolve inflammation effectively, leading to persistent inflammation and disease. Pro-inflammatory cytokines such as IL-1 and IL-18 are key mediators of inflammation in aging and age-related diseases. Their dysregulation is associated with increased inflammation and disease progression. The IL-1 family of cytokines, including IL-1α, IL-1β, and IL-18, plays a central role in the inflammatory response. IL-1β is cleaved by caspase-1 to become active, while IL-1α is activated by calpain protease. These cytokines bind to their respective receptors, triggering inflammatory signaling pathways. Age-related changes in the expression and activity of these cytokines contribute to the pro-inflammatory state seen in aging. The balance between pro-inflammatory and anti-inflammatory cytokines is crucial for maintaining immune homeostasis. Dysregulation of this balance can lead to chronic inflammation and age-related diseases. Research into the molecular pathways underlying inflammation and resolution is essential for developing new therapies to improve aging and treat age-related diseases. Potential therapeutic strategies include targeting the inflammasome, enhancing autophagy, and using pharmacological mimetics of pro-resolving mediators. Lifestyle factors, such as diet and exercise, also play a role in modulating inflammation and aging. Understanding these mechanisms is key to developing effective interventions for age-related diseases.