Hou Xiaoxiao, Wei Ziyu, Zouboulis Christos C, Ju Qiang
Department of Dermatology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Departments of Dermatology, Venereology, Allergology and Immunology, Dessau Medical Center, Brandenburg Medical School Theodor Fontane and Faculty of Health Sciences Brandenburg, Dessau, Germany.
Front Cell Dev Biol. 2022 Aug 17;10:909694. doi: 10.3389/fcell.2022.909694. eCollection 2022.
Sebaceous glands (SGs) originate from hair follicular stem cells and secrete lipids to lubricate the skin. The coordinated effects of intrinsic and extrinsic aging factors generate degradation of SGs at a late age. Senescence of SGs could be a mirror of the late aging of both the human body and skin. The procedure of SG aging goes over an initial SG hyperplasia at light-exposed skin areas to end with SG atrophy, decreased sebum secretion, and altered sebum composition, which is related to skin dryness, lack of brightness, xerosis, roughness, desquamation, and pruritus. During differentiation and aging of SGs, many signaling pathways, such as Wnt/β-catenin, c-Myc, aryl hydrocarbon receptor (AhR), and p53 pathways, are involved. Random processes lead to random cell and DNA damage due to the production of free radicals during the lifespan and neuroendocrine system alterations. Extrinsic factors include sunlight exposure (photoaging), environmental pollution, and cigarette smoking, which can directly activate signaling pathways, such as Wnt/β-catenin, Notch, AhR, and p53 pathways, and are probably associated with the de-differentiation and hyperplasia of SGs, or indirectly activate the abovementioned signaling pathways by elevating the inflammation level. The production of ROS during intrinsic SG aging is less, the signaling pathways are activated slowly and mildly, and sebocytes are still differentiated, yet terminal differentiation is not completed. With extrinsic factors, relevant signaling pathways are activated rapidly and fiercely, thus inhibiting the differentiation of progenitor sebocytes and even inducing the differentiation of progenitor sebocytes into keratinocytes. The management of SG aging is also mentioned.
皮脂腺（SGs）起源于毛囊干细胞，分泌脂质以润滑皮肤。内在和外在衰老因素的协同作用在老年时导致皮脂腺退化。皮脂腺衰老可能是人体和皮肤晚期衰老的一个反映。皮脂腺衰老过程始于暴露于光的皮肤区域最初的皮脂腺增生，最终导致皮脂腺萎缩、皮脂分泌减少和皮脂成分改变，这与皮肤干燥、缺乏光泽、皮肤干燥症、粗糙、脱屑和瘙痒有关。在皮脂腺的分化和衰老过程中，涉及许多信号通路，如Wnt/β-连环蛋白、c-Myc、芳烃受体（AhR）和p53通路。随机过程由于寿命期间自由基的产生和神经内分泌系统的改变导致随机的细胞和DNA损伤。外在因素包括阳光照射（光老化）、环境污染和吸烟，它们可直接激活信号通路，如Wnt/β-连环蛋白、Notch、AhR和p53通路，可能与皮脂腺的去分化和增生有关，或通过提高炎症水平间接激活上述信号通路。在皮脂腺内在衰老过程中活性氧的产生较少，信号通路缓慢且轻度激活，皮脂腺细胞仍在分化，但终末分化未完成。在外在因素作用下，相关信号通路迅速且强烈激活，从而抑制祖皮脂腺细胞的分化，甚至诱导祖皮脂腺细胞分化为角质形成细胞。文中还提到了皮脂腺衰老的管理。
