School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Institute of Biological Sciences (ICB), Federal University of Pará, Belem, Brazil.
Front Immunol. 2020 Oct 14;11:570083. doi: 10.3389/fimmu.2020.570083. eCollection 2020.
The aging process is driven by multiple mechanisms that lead to changes in energy production, oxidative stress, homeostatic dysregulation and eventually to loss of functionality and increased disease susceptibility. Most aged individuals develop chronic low-grade inflammation, which is an important risk factor for morbidity, physical and cognitive impairment, frailty, and death. At any age, chronic inflammatory diseases are major causes of morbimortality, affecting up to 5-8% of the population of industrialized countries. Several environmental factors can play an important role for modifying the inflammatory state. Genetics accounts for only a small fraction of chronic-inflammatory diseases, whereas environmental factors appear to participate, either with a causative or a promotional role in 50% to 75% of patients. Several of those changes depend on epigenetic changes that will further modify the individual response to additional stimuli. The interaction between inflammation and the environment offers important insights on aging and health. These conditions, often depending on the individual's sex, appear to lead to decreased longevity and physical and cognitive decline. In addition to biological factors, the environment is also involved in the generation of psychological and social context leading to stress. Poor psychological environments and other sources of stress also result in increased inflammation. However, the mechanisms underlying the role of environmental and psychosocial factors and nutrition on the regulation of inflammation, and how the response elicited for those factors interact among them, are poorly understood. Whereas certain deleterious environmental factors result in the generation of oxidative stress driven by an increased production of reactive oxygen and nitrogen species, endoplasmic reticulum stress, and inflammation, other factors, including nutrition (polyunsaturated fatty acids) and behavioral factors (exercise) confer protection against inflammation, oxidative and endoplasmic reticulum stress, and thus ameliorate their deleterious effect. Here, we discuss processes and mechanisms of inflammation associated with environmental factors and behavior, their links to sex and gender, and their overall impact on aging.
衰老过程受多种机制驱动，这些机制导致能量产生、氧化应激、内稳态失调的变化，最终导致功能丧失和疾病易感性增加。大多数老年人会出现慢性低度炎症，这是发病率、身体和认知功能障碍、虚弱和死亡的重要风险因素。在任何年龄，慢性炎症性疾病都是发病率和死亡率的主要原因，影响多达 5-8%的工业化国家人口。许多环境因素在调节炎症状态方面起着重要作用。遗传因素仅占慢性炎症性疾病的一小部分，而环境因素似乎以因果或促进作用参与其中，在 50%至 75%的患者中发挥作用。其中一些变化取决于表观遗传变化，这些变化将进一步改变个体对其他刺激的反应。炎症与环境之间的相互作用为衰老和健康提供了重要的见解。这些情况通常取决于个体的性别，似乎会导致寿命缩短和身体及认知能力下降。除了生物因素外，环境还参与产生导致压力的心理和社会环境。不良的心理环境和其他压力源也会导致炎症增加。然而，环境和社会心理因素以及营养对炎症调节的作用机制，以及这些因素对炎症反应的相互作用机制，尚不清楚。某些有害环境因素导致活性氧和氮物种、内质网应激和炎症产生增加，从而产生氧化应激，而其他因素，包括营养（多不饱和脂肪酸）和行为因素（运动），则提供了对炎症、氧化和内质网应激的保护作用，从而减轻其有害影响。在这里，我们讨论了与环境因素和行为相关的炎症过程和机制、它们与性别和性别差异的联系，以及它们对衰老的整体影响。
