Chronic inflammation is a complex and unresolved inflammatory response with low-grade multivariable patterns that aggravate systemic pathophysiological conditions and the aging process. To redefine and delineate these age-related complex inflammatory phenomena at the molecular, cellular, and systemic levels, the concept of "Senoinflammation" was recently formulated. In this review, we describe the accumulated data on both the multiphase systemic inflammatory process and the cellular proinflammatory signaling pathway. We also describe the proinflammatory mechanisms underlying the metabolic molecular pathways in aging. Additionally, we review age-related lipid accumulation, the role of the inflammatory senescence-associated secretory phenotype (SASP), the involvement of cytokine/chemokine secretion, endoplasmic reticulum (ER) stress, insulin resistance, and autophagy. The last section of the review highlights the modulation of the senoinflammatory process by the anti-aging and anti-inflammatory calorie restriction (CR). Evidence from aging and CR research strongly suggests that SASP from senescent cells may be the major source of secreted cytokines and chemokines during aging. A better understanding of the mechanisms underpinning the senoinflammatory response and the mitigating role of CR will provide insights into the molecular mechanisms of chronic inflammation and aging for potential interventions.

中文翻译：

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老年炎症：年龄相关代谢失调的主要介质。


慢性炎症是一种复杂且未解决的炎症反应，具有低级多变量模式，会加剧全身病理生理状况和衰老过程。为了在分子、细胞和系统水平上重新定义和描述这些与年龄相关的复杂炎症现象，最近提出了“老年炎症”的概念。在这篇综述中，我们描述了多相全身炎症过程和细胞促炎症信号通路的积累数据。我们还描述了衰老过程中代谢分子途径的促炎机制。此外，我们还回顾了与年龄相关的脂质积累、炎症衰老相关分泌表型 (SASP) 的作用、细胞因子/趋化因子分泌的参与、内质网 (ER) 应激、胰岛素抵抗和自噬。综述的最后一部分强调了抗衰老和抗炎热量限制（CR）对炎症过程的调节。来自衰老和 CR 研究的证据强烈表明，衰老细胞中的 SASP 可能是衰老过程中分泌的细胞因子和趋化因子的主要来源。更好地了解支持炎症反应的机制和 CR 的缓解作用，将为了解慢性炎症和衰老的分子机制提供潜在的干预措施。