Alopecia areata: What’s new in epidemiology, pathogenesis, diagnosis, and therapeutic options?

Dainichi, Teruki; Kabashima, Kenji

doi:10.1016/j.jdermsci.2016.10.004

Cited by 70 publications

(64 citation statements)

References 139 publications

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“…Patients with AA experience significant impairment in health‐related quality of life (HRQoL), with greater extent of scalp involvement associated with lower HRQoL . The disease is considered to have a multifactorial etiology involving both environmental factors, stress, and genetic susceptibility . However, the exact pathogenesis of AA still remains unknown.…”

Section: Introductionmentioning

confidence: 99%

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Identification of blood microRNA alterations in patients with severe active alopecia areata

Sheng

et al. 2019

J of Cellular Biochemistry

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Background Alopecia areata (AA) is a common inflammatory disease characterized by cellular infiltration of T cells targeting the anagen‐stage hair follicle. Lack of efficacious treatment for AA may be due to little knowledge about its exact cellular mechanism. Studies have demonstrated that microRNAs (miRNAs) play an important role in the regulation of inflammatory skin diseases such as atopic dermatitis and psoriasis. However, little is known about the role of miRNAs in AA. Objective The present study aimed to explore the blood miRNAs alterations in patients with severe active AA. Methods We constructed a bipartite miRNA‐messenger RNA (mRNA) regulatory network by the validated miRNA‐mRNA relationships. Subsequently, the miRNA‐miRNA synergistic network was formed in consideration of the Gene Ontology function enrichment of coregulated target genes. Lastly, the functional network was identified by the ingenuity pathway analysis. Results By using an Agilent microarray that covers 2549 human miRNAs, we identified 36 significantly differentially expressed miRNAs in severe active AA patients. miRNA target gene prediction and functional annotation analysis showed significant enrichment in several pathways including the ribosome, cancer, cell cycle, insulin signaling, transforming growth factor‐βsignaling, and p53 signaling pathways. Analysis of the three kinds of network showed that miR‐185‐5p, miR‐125b‐5p, and miR‐186‐5p might play important and synergistic roles in the active phase of AA. According to the receiver operating characteristic curve analysis, several miRNAs were selected for the quantitative real‐time polymerase chain reaction validation. Among the miRNAs, miR‐210 and miR‐1246 had high prediction with high accuracy. Conclusion Blood dysregulated miRNAs are potentially associated with the severe active AA. These miRNAs could function synergistically and might be promising targets for the development of novel treatments for AA in the future.

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Section: Introductionmentioning

confidence: 99%

“…2,3 The disease is considered to have a multifactorial etiology involving both environmental factors, stress, and genetic susceptibility. [4][5][6][7] However, the exact pathogenesis of AA still remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Identification of blood microRNA alterations in patients with severe active alopecia areata

Sheng

et al. 2019

J of Cellular Biochemistry

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“…About 2% of cases spread to the entire scalp (alopecia totalis) or body (alopecia universalis) [2]. An incidence of [ 2% among the general population has been reported, with a lifetime risk of 1.7% for both men and women [3]. AA is mainly related to genetic, autoimmunity and inflammatory factors [4,5], with the collapse of the immune privilege of the hair follicle reported to play a pivotal role in the pathogenesis of this autoimmune disorder [6].…”

Section: Introductionmentioning

confidence: 99%

Efficacy of Postbiotics in a PRP-Like Cosmetic Product for the Treatment of Alopecia Area Celsi: A Randomized Double-Blinded Parallel-Group Study

Rinaldi

Trink

Pinto

2020

Dermatol Ther (Heidelb)

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“…Current hypotheses for AA development include genetic predisposition with inflammatory receptors and cytokines (cytotoxic T-lymphocyte-associated protein 4, tumor necrosis factor [TNF], interleukin 13, TNF superfamily member 4, chemokine ligands 9 and 10, and toll-like receptor 1) causing dysregulation of T-cell differentiation, increasing T-helper 17 cells, and decreasing T-regulatory cells [4]. Other causes include disturbances in immune privilege with hair follicle destruction, autoantibodies against tyrosine hydroxylase and retinol-binding protein 4, and vitamin irregularities including high retinoic acid and low vitamin D [4].…”

Section: Introductionmentioning

confidence: 99%

“…Other causes include disturbances in immune privilege with hair follicle destruction, autoantibodies against tyrosine hydroxylase and retinol-binding protein 4, and vitamin irregularities including high retinoic acid and low vitamin D [4]. Further evidence for immune dysregulation in AA comes from recently developed mouse models, in which transferring a single CD8+ T-cell clone or lymph-node-derived cell from an alopecia-affected to an unaffected mouse induces hair loss in the healthy subject [4]. …”

Section: Introductionmentioning

confidence: 99%

Does Complement Have a Role in the Pathogenesis of Alopecia Areata?

Juhász

Mesinkovska²

2018

Skin Appendage Disord

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Alopecia areata (AA) is an autoimmune disorder in which immune attack of the anagen follicle causes hair loss in approximately 2% of the population. Although the pathogenesis of AA has not been fully determined, most likely it is mediated by a variety of factors including cellular/humoral immunity and genetic predisposition. Researchers have been interested in the possible role of the complement pathway in AA since the 1970s. Given recent evidence suggesting that complement plays a role in many immunologic and inflammatory dermatologic diseases including systemic lupus erythematosus, bullous diseases, angioedema, lipodystrophy, and skin infections, it is likely that complement also contributes to AA pathogenesis. Although early serum studies and immunohistochemical staining have been unimpressive, recent genetics studies may provide evidence that complement does indeed contribute to AA. By determining if complement plays a role in AA, options for novel targeted treatments will become available for those patients with refractory disease.

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Alopecia areata: What’s new in epidemiology, pathogenesis, diagnosis, and therapeutic options?

Cited by 70 publications

References 139 publications

Identification of blood microRNA alterations in patients with severe active alopecia areata

Identification of blood microRNA alterations in patients with severe active alopecia areata

Efficacy of Postbiotics in a PRP-Like Cosmetic Product for the Treatment of Alopecia Area Celsi: A Randomized Double-Blinded Parallel-Group Study

Does Complement Have a Role in the Pathogenesis of Alopecia Areata?

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