Frontal fibrosing alopecia: A review of disease pathogenesis.
Frontal fibrosing alopecia: A review of disease pathogenesis.
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DOI：
10.3389/fmed.2022.911944
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发表时间：
2022
影响因子：
3.9
通讯作者：
中科院分区：
文献类型：
--
作者：
额部纤维性脱发（FFA）是一种主要影响绝经后妇女的原发性瘢痕性脱发，可引起额颞部发际线后退和眉毛脱落。尽管FFA的发病率在过去十年中在全球范围内增加，但其病因和病理仍不清楚。我们涵盖了其病理生理学的最新发现，包括免疫调节，神经源性炎症和遗传调控，为当前的临床治疗提供更多的选择。持续的炎症反应和免疫赦免（IP）崩溃发展并导致上皮毛囊干细胞（eHFSC）破坏和隆突区的上皮-间充质转化（EMT），这是FFA发病的关键过程。最终，纤维组织取代正常的上皮组织并填充整个毛囊（HF）。此外，一些家族性报告和全基因组关联研究表明FFA的发病存在遗传易感性或表观遗传机制。FFA的发病率在绝经后妇女中急剧增加，并且临床观察中许多FFA患者还患有女性型脱发，这表明FFA与类固醇激素之间存在潜在的关联。阳光照射和局部过敏原也可能是FFA的触发因素，但这一猜想尚未得到证实。需要更多的证据和队列研究来帮助我们了解这种疾病的发病机制。不同的假设触发因素，如香皂，化妆品，防晒霜或压力条件，可能会导致潜在遗传易感个体的FFA。PPAR-γ/TGF-β通路在EMT和纤维化中起重要作用。mTOR信号传导作为PPAR-γ活性和脂质稳态的调节剂起作用。箭头和线条表示两种元素之间的规则关系：mTOR：雷帕霉素的哺乳动物靶标; PPAR-γ：过氧化物酶体增殖物激活受体γ; DHEA：脱氢表雄酮; HF：毛囊; IFN：干扰素; TGF-β：转化生长因子-β; IP：免疫赦免; EMT：上皮-间质转化; SP：P物质; NK-1：神经激肽-1。创建于BioRender.com（于二零二二年二月七日访问）。
Frontal fibrosing alopecia (FFA) is a primary patterned cicatricial alopecia that mostly affects postmenopausal women and causes frontotemporal hairline regression and eyebrow loss. Although the incidence of FFA has increased worldwide over the last decade, its etiology and pathology are still unclear. We cover the latest findings on its pathophysiology, including immunomodulation, neurogenic inflammation, and genetic regulation, to provide more alternatives for current clinical treatment. A persistent inflammatory response and immune privilege (IP) collapse develop and lead to epithelial hair follicle stem cells (eHFSCs) destruction and epithelial-mesenchymal transition (EMT) in the bulge area, which is the key process in FFA pathogenesis. Eventually, fibrous tissue replaces normal epithelial tissue and fills the entire hair follicle (HF). In addition, some familial reports and genome-wide association studies suggest a genetic susceptibility or epigenetic mechanism for the onset of FFA. The incidence of FFA increases sharply in postmenopausal women, and many FFA patients also suffer from female pattern hair loss in clinical observation, which suggests a potential association between FFA and steroid hormones. Sun exposure and topical allergens may also be triggers of FFA, but this conjecture has not been proven. More evidence and cohort studies are needed to help us understand the pathogenesis of this disease. Different hypothetical triggers, such as facial soap, cosmetics, sunscreen, or stressful conditions, can cause FFA in potentially genetically susceptible individuals. PPAR-γ/TGF-β pathway plays an essential role in EMT and fibrosis. mTOR signaling works as a modulator of PPAR-γ activity and lipid homeostasis. Arrows and lines indicate a regular relationship between two elements mTOR: mammalian target of rapamycin; PPAR-γ: peroxisome proliferator-activated receptor γ; DHEA: dehydroepiandrosterone; HF: hair follicle; IFN: interferon; TGF-β: transforming growth factor-β; IP: immune privilege; EMT: epithelial-mesenchymal transition; SP: substance P; NK-1: Neurokinin-1. Created with BioRender.com (accessed on 7 February 2022).
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影响因子：
27.4
作者：
Gonzalez, Estrella Garcia;Selvi, Enrico;Distler, Joerg H. W.
通讯作者：
Distler, Joerg H. W.
影响因子：
7.3
作者：
Harries, Matthew J.;Meyer, Katja;Paus, Ralf
通讯作者：
Paus, Ralf
影响因子：
6.5
作者：
Imanishi, Hisayoshi;Ansell, David M.;Paus, Ralf
通讯作者：
Paus, Ralf
影响因子：
6.5
作者：
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通讯作者：
Mirmirani, Paradi
影响因子：
3.6
作者：
Doche, Isabella;Wilcox, George L.;Hordinsky, Maria K.
通讯作者：
Hordinsky, Maria K.