Cellular Senescence: The Hidden Driver In Chronic Inflammatory Skin Disorders
For a long time, scientists believed that chronic inflammatory skin conditions, which cause persistent skin inflammation, a weakened skin barrier, and frequent flare-ups, were primarily due to problems with the immune system. However, emerging evidence points to a “hidden driver” behind these stubborn skin issues: cellular senescence. This is a state where cells permanently stop dividing, often due to stress or damage. These senescent cells aren’t just dormant; they actively release a mix of inflammatory molecules, growth factors, and enzymes, collectively known as the senescence-associated secretory phenotype (SASP). This SASP creates a pro-inflammatory environment that can damage surrounding healthy tissues and sustain chronic inflammation. For instance, when skin cells called keratinocytes become senescent, they can disrupt the skin’s protective barrier, leading to thinning and dryness. Similarly, senescent fibroblasts, which are crucial for skin structure, can break down the skin’s support network and attract immune cells, further fueling inflammation. Understanding this process opens up new avenues for treatment, potentially by developing therapies that specifically target and remove these senescent cells, offering a fresh approach to managing these challenging skin disorders.
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