分子炎症：衰老及与年龄相关疾病的基础
Molecular inflammation: underpinnings of aging and age-related diseases.
作者信息
Chung Hae Young, Cesari Matteo, Anton Stephen, Marzetti Emanuele, Giovannini Silvia, Seo Arnold Young, Carter Christy, Yu Byung Pal, Leeuwenburgh Christiaan
机构信息
Department of Pharmacy, Longevity Science and Technology Institutes, Research Institute for Drug Development, Pusan National University, Geumjeong-gu, Busan 609-735, South Korea.
出版信息
Ageing Res Rev. 2009 Jan;8(1):18-30. doi: 10.1016/j.arr.2008.07.002. Epub 2008 Jul 18.
Recent scientific studies have advanced the notion of chronic inflammation as a major risk factor underlying aging and age-related diseases. In this review, low-grade, unresolved, molecular inflammation is described as an underlying mechanism of aging and age-related diseases, which may serve as a bridge between normal aging and age-related pathological processes. Accumulated data strongly suggest that continuous (chronic) upregulation of pro-inflammatory mediators (e.g., TNF-alpha, IL-1beta, IL-6, COX-2, iNOS) are induced during the aging process due to an age-related redox imbalance that activates many pro-inflammatory signaling pathways, including the NF-kappaB signaling pathway. These pro-inflammatory molecular events are discussed in relation to their role as basic mechanisms underlying aging and age-related diseases. Further, the anti-inflammatory actions of aging-retarding caloric restriction and exercise are reviewed. Thus, the purpose of this review is to describe the molecular roles of age-related physiological functional declines and the accompanying chronic diseases associated with aging. This new view on the role of molecular inflammation as a mechanism of aging and age-related pathogenesis can provide insights into potential interventions that may affect the aging process and reduce age-related diseases, thereby promoting healthy longevity.
最近的科学研究提出了慢性炎症这一概念，认为它是衰老及与年龄相关疾病的主要风险因素。在本综述中，低度、未消退的分子炎症被描述为衰老及与年龄相关疾病的潜在机制，它可能是正常衰老与和年龄相关的病理过程之间的桥梁。大量数据有力地表明，由于与年龄相关的氧化还原失衡激活了包括NF-κB信号通路在内的许多促炎信号通路，在衰老过程中会诱导促炎介质（如肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-6、环氧化酶-2、诱导型一氧化氮合酶）持续（慢性）上调。本文讨论了这些促炎分子事件作为衰老及与年龄相关疾病潜在机制的作用。此外，还综述了延缓衰老的热量限制和运动的抗炎作用。因此，本综述的目的是描述与年龄相关的生理功能衰退以及伴随衰老出现的慢性疾病的分子作用。这种关于分子炎症作为衰老和与年龄相关发病机制的新观点，能够为可能影响衰老过程并减少与年龄相关疾病的潜在干预措施提供见解，从而促进健康长寿。
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