Adipose Immune Microenvironment: Catalyst Of Age-Related Adipose Tissue Dysfunction
As we age, our bodies undergo many changes, and our fat tissue is no exception. This tissue, often seen simply as a storage for energy, is actually a dynamic organ with its own complex immune system. With age, this internal immune environment within our fat tissue changes dramatically, leading to a state of chronic, low-grade inflammation. This inflammation is a key factor in why our fat tissue starts to malfunction as we get older.
These age-related changes disrupt the delicate balance and metabolic functions of fat tissue, which can contribute to various age-related diseases. Specifically, certain immune components, like the NLRP3 inflammasome, become overactive in response to cellular damage, driving further dysfunction and an increase in problematic immune cells. These dysfunctional immune cells and other pro-inflammatory cells work together, creating a cycle that promotes ongoing inflammation and metabolic issues. Additionally, the signaling molecules produced by fat cells, called adipokines, are altered with age, further throwing off the immune and metabolic balance.
Understanding these intricate interactions between immune cells and adipokines in aging fat tissue is crucial. By identifying these mechanisms, researchers can explore new ways to target this inflammation, aiming to improve fat tissue function and promote healthier aging overall.
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