How Inflammation Causes Aging

Controlling intestinal inflammation could be one way to prevent aging, at least in mice.

AsianScientist (Jan. 27, 2017) – Researchers from South Korea have identified the mechanisms behind how chronic, low-grade inflammation causes aging. Their results have been published in Scientific Reports.

Although inflammation has been proposed to cause aging in theory, it has not been decisively been proven. In the current study, a team led by Chair-Professor Park Sang-Cheol from Daegu Gyeongbuk Institute of Science and Technology has found that inflammation weakens the blood vessels as mice age.

They showed that supportive cells surrounding endothelial cells in the intestinal tissues decreased as the mice grew older. This in turn caused blood vessel function to deteriorate, worsening to the point of vascular leakage.

Upon further investigation, the researchers found that this phenomenon is due to the increase of gut-resident inflammatory cells (macrophages) and the increase of TNF-α, cytokine secreted by these cells, which caused changes in the surrounding environment of blood vessel.

“This study is significant as we have newly identified the mechanisms of aging associated with inflammation increase and opened possibilities of applied researches on aging delay through inflammation control as well as anti-aging,” said Park.

“We will conduct follow-up studies to find ways to extend human health life by controlling inflammatory cells and vascular leakage to delay aging.”

Follow-up studies on intestinal inflammation control could help the development of various technologies that can practically delay aging. Park and his team are currently exploring a variety of candidate substances that are able to control gut-resident inflammation with the aim of clinical studies.

The article can be found at: Jeong et al. (2017) Microvasculature Remodeling in the Mouse Lower Gut During Inflammaging.


Source: Daegu Gyeongbuk Institute of Science and Technology; Photo: Pixabay.
Disclaimer: This article does not necessarily reflect the views of AsianScientist or its staff.

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