{"id":243158,"date":"2026-08-25T05:02:30","date_gmt":"2026-08-25T10:02:30","guid":{"rendered":"https:\/\/lifeboat.com\/blog\/2026\/08\/noncircadian-bmal1yap-activity-amplifies-persistent-inflammation-in-aged-epidermis-aging"},"modified":"2026-08-25T05:02:30","modified_gmt":"2026-08-25T10:02:30","slug":"noncircadian-bmal1yap-activity-amplifies-persistent-inflammation-in-aged-epidermis-aging","status":"publish","type":"post","link":"https:\/\/lifeboat.com\/blog\/2026\/08\/noncircadian-bmal1yap-activity-amplifies-persistent-inflammation-in-aged-epidermis-aging","title":{"rendered":"Noncircadian BMAL1YAP activity amplifies persistent inflammation in aged epidermis Aging"},"content":{"rendered":"<p style=\"padding-right: 20px\"><a class=\"aligncenter blog-photo\" href=\"https:\/\/lifeboat.com\/blog.images\/noncircadian-bmal1yap-activity-amplifies-persistent-inflammation-in-aged-epidermis-aging.jpg\"><\/a><\/p>\n<p>Researchers have identified a cellular \u201caging switch\u201d driving age-related skin decline and chronic inflammation, centered on the interaction between two proteins, BMAL1 and YAP. While these proteins independently maintain cellular structure in youth, age-related tissue stiffening and the immune signaling protein Interleukin-17 (IL-17) cause them to alter their behavior, binding to new DNA regions to aggressively activate inflammatory genes and impair wound healing. In a study published in <i><i>Nature<\/i> Aging<\/i>, experiments on mice demonstrated that temporarily blocking IL-17 suppressed this BMAL1-YAP inflammatory pathway and significantly reversed visible signs of skin aging, highlighting a promising new therapeutic target for treating age-related epidermal deterioration in humans.<\/p>\n<hr>\n<p>Chronic inflammation is a hallmark of aging, yet the underlying molecular mechanisms are incompletely understood. Here the authors show that, in the skin, BMAL1 and YAP cooperate at enhancers to maintain epidermal homeostasis. During aging, this cooperation is increased at inflammatory enhancers, driven by age-associated changes in the microenvironment, promoting epidermal inflammation.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Researchers have identified a cellular \u201caging switch\u201d driving age-related skin decline and chronic inflammation, centered on the interaction between two proteins, BMAL1 and YAP. While these proteins independently maintain cellular structure in youth, age-related tissue stiffening and the immune signaling protein Interleukin-17 (IL-17) cause them to alter their behavior, binding to new DNA regions to [\u2026]<\/p>\n","protected":false},"author":461,"featured_media":0,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[11,269],"tags":[],"class_list":["post-243158","post","type-post","status-publish","format-standard","hentry","category-biotech-medical","category-life-extension"],"_links":{"self":[{"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/posts\/243158","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/users\/461"}],"replies":[{"embeddable":true,"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/comments?post=243158"}],"version-history":[{"count":0,"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/posts\/243158\/revisions"}],"wp:attachment":[{"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/media?parent=243158"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/categories?post=243158"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/lifeboat.com\/blog\/wp-json\/wp\/v2\/tags?post=243158"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}