Fat tissue, a major organ in humans, is central to aging and age-related metabolic dysfunction. It undergoes significant changes throughout life, with obesity linked to accelerated onset of age-related diseases, while fat reduction or mutations can extend lifespan. Fat cells continuously turnover, and preadipocytes, which are abundant and closely related to macrophages, become dysdifferentiated with age, adopting a pro-inflammatory, senescent-like state. Other mesenchymal progenitors can also acquire a pro-inflammatory, adipocyte-like phenotype with aging. A model suggests that cellular stress and preadipocyte overutilization with aging induce cellular senescence, leading to impaired adipogenesis, failure to sequester lipotoxic fatty acids, and increased inflammatory cytokines and immune responses. These processes may amplify each other and have systemic consequences. Cellular senescence is a stress-responsive, adaptive phenotype that can develop through multiple stages, including metabolic and secretory adjustments, and can spread from cell to cell. Senescence can occur in both dividing and non-dividing cells in response to injury or metabolic dysfunction. Senescent-like states can develop in non-replicating, differentiated cells in fat tissue, challenging existing concepts about cellular senescence. Fat tissue is important for energy storage, immune and endocrine function, thermoregulation, and tissue regeneration. It is rich in mesenchymal progenitors that can give rise to multiple cell types, including fat cells. Fat tissue dysfunction is associated with metabolic syndrome, inflammation, and reduced longevity. Obesity is linked to accelerated fat tissue aging, with increased inflammation, insulin resistance, and ectopic lipid deposition. Fat tissue inflammation in obesity is associated with shifts in T-lymphocyte subsets, mast cell infiltration, and activation of M1 macrophages. These processes may contribute to age-related fat tissue dysfunction and metabolic disease. Preadipocytes are a major progenitor pool in fat tissue, with distinct subtypes in different fat depots. Aging and obesity both affect preadipocyte function, leading to reduced adipogenesis, increased pro-inflammatory cytokines, and cellular senescence. Preadipocytes can become macrophage-like or progress along the adipocytic lineage. Cellular senescence in fat tissue is associated with increased SA β-gal activity, p53, and other markers. Senescent cells can contribute to systemic inflammation and metabolic dysfunction. Obesity and aging are associated with increased senescent cells in fat tissue, which may lead to immune cell infiltration and pro-inflammatory states. Cellular senescence in fat tissue is linked to increased inflammation, insulin resistance, and metabolic disease. Fat tissue inflammation and cellular senescence with aging are associated with increased pro-inflammatory cytokines, such as TNFα and IL-6, and may contribute to age-related diseases. Fat tissue dysfunction in aging is linked to reduced adipogenesis, increased lipotoxicity, and metabolic syndrome. Fat tissue inflammation in obesityFat tissue, a major organ in humans, is central to aging and age-related metabolic dysfunction. It undergoes significant changes throughout life, with obesity linked to accelerated onset of age-related diseases, while fat reduction or mutations can extend lifespan. Fat cells continuously turnover, and preadipocytes, which are abundant and closely related to macrophages, become dysdifferentiated with age, adopting a pro-inflammatory, senescent-like state. Other mesenchymal progenitors can also acquire a pro-inflammatory, adipocyte-like phenotype with aging. A model suggests that cellular stress and preadipocyte overutilization with aging induce cellular senescence, leading to impaired adipogenesis, failure to sequester lipotoxic fatty acids, and increased inflammatory cytokines and immune responses. These processes may amplify each other and have systemic consequences. Cellular senescence is a stress-responsive, adaptive phenotype that can develop through multiple stages, including metabolic and secretory adjustments, and can spread from cell to cell. Senescence can occur in both dividing and non-dividing cells in response to injury or metabolic dysfunction. Senescent-like states can develop in non-replicating, differentiated cells in fat tissue, challenging existing concepts about cellular senescence. Fat tissue is important for energy storage, immune and endocrine function, thermoregulation, and tissue regeneration. It is rich in mesenchymal progenitors that can give rise to multiple cell types, including fat cells. Fat tissue dysfunction is associated with metabolic syndrome, inflammation, and reduced longevity. Obesity is linked to accelerated fat tissue aging, with increased inflammation, insulin resistance, and ectopic lipid deposition. Fat tissue inflammation in obesity is associated with shifts in T-lymphocyte subsets, mast cell infiltration, and activation of M1 macrophages. These processes may contribute to age-related fat tissue dysfunction and metabolic disease. Preadipocytes are a major progenitor pool in fat tissue, with distinct subtypes in different fat depots. Aging and obesity both affect preadipocyte function, leading to reduced adipogenesis, increased pro-inflammatory cytokines, and cellular senescence. Preadipocytes can become macrophage-like or progress along the adipocytic lineage. Cellular senescence in fat tissue is associated with increased SA β-gal activity, p53, and other markers. Senescent cells can contribute to systemic inflammation and metabolic dysfunction. Obesity and aging are associated with increased senescent cells in fat tissue, which may lead to immune cell infiltration and pro-inflammatory states. Cellular senescence in fat tissue is linked to increased inflammation, insulin resistance, and metabolic disease. Fat tissue inflammation and cellular senescence with aging are associated with increased pro-inflammatory cytokines, such as TNFα and IL-6, and may contribute to age-related diseases. Fat tissue dysfunction in aging is linked to reduced adipogenesis, increased lipotoxicity, and metabolic syndrome. Fat tissue inflammation in obesity