Fig. 8: Schematic overview of main findings demonstrating that targeting enhanced IL-36R signaling in aged skin keratinocytes alleviates traumatic OA progression in mice. | Nature Communications

Fig. 8: Schematic overview of main findings demonstrating that targeting enhanced IL-36R signaling in aged skin keratinocytes alleviates traumatic OA progression in mice.

From: Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling

Fig. 8: Schematic overview of main findings demonstrating that targeting enhanced IL-36R signaling in aged skin keratinocytes alleviates traumatic OA progression in mice.The alternative text for this image may have been generated using AI.

IL-36Ra decreases in senescent epidermal keratinocytes of aged mice and patients, which leads to age-related low-level inflammatory with increased secretion of IL-36 agonizts, activated pro-inflammatory signaling, and promoted senescence in chondrocytes and synovial fibroblasts. Deletion of IL-36Ra in keratinocytes aggravates experimental and age-related OA in mice, whereas mIL-36Ra treatment or deletion of IL-36R effectively attenuates OA progression. Insertion of mIL-36Ra or spesolimab loaded microneedles into skin provides prolonged inhibition of IL-36R signaling directly in skin keratinocytes, representing a promising drug delivery system to broaden the usage of IL-36Ra in clinical OA treatment.

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