Tang Yizhe, Purkayastha Sudarshana, Cai Dongsheng
Department of Molecular Pharmacology, Diabetes Research Center, Institute of Aging, Albert Einstein College of Medicine, New York, NY 10461, USA.
Department of Molecular Pharmacology, Diabetes Research Center, Institute of Aging, Albert Einstein College of Medicine, New York, NY 10461, USA.
Trends Neurosci. 2015 Jan;38(1):36-44. doi: 10.1016/j.tins.2014.10.002. Epub 2014 Nov 14.
Chronic microinflammation is a hallmark of many aging-related neurodegenerative diseases as well as metabolic syndrome-driven diseases. Recent research indicates that chronic caloric excess can lead to hypothalamic microinflammation, which in turn participates in the development and progression of metabolic syndrome disorders such as obesity, glucose intolerance, and hypertension. Additionally, it was recently shown that increasing age after young adulthood can cause hypothalamic microinflammation independently of nutritional status, mediating a central mechanism of systemic aging. Taken together, these findings suggest that the hypothalamus has a fundamental role, via hypothalamic microinflammation, in translating overnutrition and aging into complex outcomes. Here we summarize recent work and suggest a conceptual model in which hypothalamic microinflammation is a common mediator of metabolic syndrome and aging.
慢性微炎症是许多与衰老相关的神经退行性疾病以及代谢综合征驱动疾病的一个标志。最近的研究表明，长期热量摄入过多会导致下丘脑微炎症，进而参与肥胖、葡萄糖不耐受和高血压等代谢综合征疾病的发生和发展。此外，最近有研究表明，成年后年龄增长会独立于营养状况引发下丘脑微炎症，介导全身衰老的核心机制。综上所述，这些发现表明，下丘脑通过下丘脑微炎症在将营养过剩和衰老转化为复杂后果方面具有重要作用。在此，我们总结了近期的研究工作，并提出一个概念模型，其中下丘脑微炎症是代谢综合征和衰老的共同介导因素。
