Obesity represents a serious health problem as it is rapidly increasing worldwide. Obesity is associated with reduced healthspan and lifespan, decreased responses to infections and vaccination, and increased frequency of inflammatory conditions typical of old age. Obesity is characterized by increased fat mass and remodeling of the adipose tissue (AT). In this review, we summarize published data on the different types of AT present in mice and humans, and their roles as fat storage as well as endocrine and immune tissues. We review the age-induced changes, including those in the distribution of fat in the body, in abundance and function of adipocytes and their precursors, and in the infiltration of immune cells from the peripheral blood. We also show that cells with a senescent-associated secretory phenotype accumulate in the AT of mice and humans with age, where they secrete several factors involved in the establishment and maintenance of local inflammation, oxidative stress, cell death, tissue remodeling, and infiltration of pro-inflammatory immune cells. Not only adipocytes and pre-adipocytes but also immune cells show a senescent phenotype in the AT. With the increase in human lifespan, it is crucial to identify strategies of intervention and target senescent cells in the AT to reduce local and systemic inflammation and the development of age-associated diseases. Several studies have indeed shown that senescent cells can be effectively targeted in the AT by selectively removing them or by inhibiting the pathways that lead to the secretion of pro-inflammatory factors.

肥胖是一个严重的健康问题，因为它在全球范围内迅速增加。肥胖与健康寿命和寿命缩短、对感染和疫苗接种的反应降低以及老年典型炎症状况的频率增加有关。肥胖的特征是脂肪量增加和脂肪组织 (AT) 的重塑。在这篇综述中，我们总结了关于小鼠和人类中不同类型 AT 的已发表数据，以及它们作为脂肪储存以及内分泌和免疫组织的作用。我们回顾了年龄引起的变化，包括体内脂肪分布、脂肪细胞及其前体的丰度和功能以及外周血免疫细胞浸润的变化。我们还表明，随着年龄的增长，具有衰老相关分泌表型的细胞会在小鼠和人类的 AT 中积累，在那里它们会分泌多种参与局部炎症、氧化应激、细胞死亡、组织重塑和浸润的因子。促炎免疫细胞。不仅脂肪细胞和前脂肪细胞而且免疫细胞在 AT 中都显示出衰老表型。随着人类寿命的延长，确定干预策略和靶向 AT 中的衰老细胞以减少局部和全身炎症以及与年龄相关疾病的发展至关重要。几项研究确实表明，通过选择性去除它们或抑制导致促炎因子分泌的途径，可以有效地靶向 AT 中的衰老细胞。它们分泌多种因子，参与局部炎症、氧化应激、细胞死亡、组织重塑和促炎免疫细胞浸润的建立和维持。不仅脂肪细胞和前脂肪细胞而且免疫细胞在 AT 中都显示出衰老表型。随着人类寿命的延长，确定干预策略和靶向 AT 中的衰老细胞以减少局部和全身炎症以及与年龄相关疾病的发展至关重要。几项研究确实表明，通过选择性去除它们或抑制导致促炎因子分泌的途径，可以有效地靶向 AT 中的衰老细胞。它们分泌多种因子，参与局部炎症、氧化应激、细胞死亡、组织重塑和促炎免疫细胞浸润的建立和维持。不仅脂肪细胞和前脂肪细胞而且免疫细胞在 AT 中都显示出衰老表型。随着人类寿命的延长，确定干预策略和靶向 AT 中的衰老细胞以减少局部和全身炎症以及与年龄相关疾病的发展至关重要。几项研究确实表明，通过选择性去除它们或抑制导致促炎因子分泌的途径，可以有效地靶向 AT 中的衰老细胞。细胞死亡、组织重塑和促炎免疫细胞浸润。不仅脂肪细胞和前脂肪细胞而且免疫细胞在 AT 中都显示出衰老表型。随着人类寿命的延长，确定干预策略和靶向 AT 中的衰老细胞以减少局部和全身炎症以及与年龄相关疾病的发展至关重要。几项研究确实表明，通过选择性去除它们或抑制导致促炎因子分泌的途径，可以有效地靶向 AT 中的衰老细胞。细胞死亡、组织重塑和促炎免疫细胞浸润。不仅脂肪细胞和前脂肪细胞而且免疫细胞在 AT 中都显示出衰老表型。随着人类寿命的延长，确定干预策略和靶向 AT 中的衰老细胞以减少局部和全身炎症以及与年龄相关疾病的发展至关重要。几项研究确实表明，通过选择性去除它们或抑制导致促炎因子分泌的途径，可以有效地靶向 AT 中的衰老细胞。确定干预策略和靶向 AT 中的衰老细胞以减少局部和全身炎症以及与年龄相关疾病的发展至关重要。几项研究确实表明，通过选择性去除它们或抑制导致促炎因子分泌的途径，可以有效地靶向 AT 中的衰老细胞。确定干预策略和靶向 AT 中的衰老细胞以减少局部和全身炎症以及与年龄相关疾病的发展至关重要。几项研究确实表明，通过选择性去除它们或抑制导致促炎因子分泌的途径，可以有效地靶向 AT 中的衰老细胞。