Wounding Therapies for Prevention of Photocarcinogenesis.

Wounding Therapies for Prevention of Photocarcinogenesis.
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DOI:
10.3389/fonc.2021.813132
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发表时间:
2021
影响因子:
4.7
通讯作者:
Travers JB
Travers JB
中科院分区:
医学3区
文献类型:
--
作者:
Frommeyer TC;Rohan CA;Spandau DF;Kemp MG;Wanner MA;Tanzi E;Travers JB

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非黑色素瘤皮肤癌(NMSC)的发生与高龄和紫外线B(UVB)暴露密切相关。更具体地说,NMSC的发育与老年皮肤中衰老真皮成纤维细胞的胰岛素样生长因子-1(IGF-1)信号转导减少有关。因此,角质形成细胞IGF-1受体(IGF-1 R)保持无活性,导致无法诱导适当的保护性反应,包括DNA修复和细胞周期检查点信号传导。这使得UVB诱导的DNA损伤不受抑制地增殖,从而增加了恶性转化的可能性。据估计,NMSC每年发生在330万人中。发病率的上升导致发病率增加和医疗保健费用增加,这需要确定有效的治疗方式。在这篇综述中,我们强调了NMSC的发病机制,并讨论了新的预防性治疗的潜力。特别是,创伤治疗,如磨皮,微针,化学脱皮,和分段激光换肤已被证明可以恢复老年皮肤中的IGF-1/IGF-1 R信号传导,并抑制UVB损伤的角质形成细胞的繁殖。这种创伤反应有效地使老年皮肤恢复活力,并降低与年龄相关的NMSC的发病率。
The occurrence of non-melanoma skin cancer (NMSC) is closely linked with advanced age and ultraviolet-B (UVB) exposure. More specifically, the development of NMSC is linked to diminished insulin-like growth factor-1 (IGF-1) signaling from senescent dermal fibroblasts in geriatric skin. Consequently, keratinocyte IGF-1 receptor (IGF-1R) remains inactive, resulting in failure to induce appropriate protective responses including DNA repair and cell cycle checkpoint signaling. This allows UVB-induced DNA damage to proliferate unchecked, which increases the likelihood of malignant transformation. NMSC is estimated to occur in 3.3 million individuals annually. The rising incidence results in increased morbidity and significant healthcare costs, which necessitate identification of effective treatment modalities. In this review, we highlight the pathogenesis of NMSC and discuss the potential of novel preventative therapies. In particular, wounding therapies such as dermabrasion, microneedling, chemical peeling, and fractionated laser resurfacing have been shown to restore IGF-1/IGF-1R signaling in geriatric skin and suppress the propagation of UVB-damaged keratinocytes. This wounding response effectively rejuvenates geriatric skin and decreases the incidence of age-associated NMSC.
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