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      Androgenetic Alopecia: Therapy Update

      review-article

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          Abstract

          Androgenetic alopecia (AGA), also known as male pattern hair loss (MPHL) or female pattern hair loss (FPHL), is the most common form of alopecia worldwide, and arises from an excessive response to androgens. AGA presents itself in a characteristic distribution unique to both sexes. Despite its prevalence, AGA can be quite challenging to treat. The condition is chronic in nature and stems from an interplay of genetic and environmental factors. There are only two US Food and Drug Administration (FDA)-approved drugs for the condition: topical minoxidil and oral finasteride. However, numerous non-FDA-approved treatments have been shown to be effective in treating AGA in various studies. Some of these treatments are relatively new and still to be explored, thus emphasizing the need for an updated review of the literature. In this comprehensive review, we discuss the evaluation of AGA and the mechanisms of action, costs, efficacies, and safety profiles of existing, alternative, and upcoming therapeutics for this widespread condition.

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          Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition.

          Luzhou Xing, Zhenpeng Dai, Ali Jabbari … (2014)
          Alopecia areata (AA) is a common autoimmune disease resulting from damage of the hair follicle by T cells. The immune pathways required for autoreactive T cell activation in AA are not defined limiting clinical development of rational targeted therapies. Genome-wide association studies (GWAS) implicated ligands for the NKG2D receptor (product of the KLRK1 gene) in disease pathogenesis. Here, we show that cytotoxic CD8(+)NKG2D(+) T cells are both necessary and sufficient for the induction of AA in mouse models of disease. Global transcriptional profiling of mouse and human AA skin revealed gene expression signatures indicative of cytotoxic T cell infiltration, an interferon-γ (IFN-γ) response and upregulation of several γ-chain (γc) cytokines known to promote the activation and survival of IFN-γ-producing CD8(+)NKG2D(+) effector T cells. Therapeutically, antibody-mediated blockade of IFN-γ, interleukin-2 (IL-2) or interleukin-15 receptor β (IL-15Rβ) prevented disease development, reducing the accumulation of CD8(+)NKG2D(+) T cells in the skin and the dermal IFN response in a mouse model of AA. Systemically administered pharmacological inhibitors of Janus kinase (JAK) family protein tyrosine kinases, downstream effectors of the IFN-γ and γc cytokine receptors, eliminated the IFN signature and prevented the development of AA, while topical administration promoted hair regrowth and reversed established disease. Notably, three patients treated with oral ruxolitinib, an inhibitor of JAK1 and JAK2, achieved near-complete hair regrowth within 5 months of treatment, suggesting the potential clinical utility of JAK inhibition in human AA.
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            Exosomes from mesenchymal stem/stromal cells: a new therapeutic paradigm

            Kan Yin, Shihua Wang, Robert Chunhua Zhao (2019)
            Mesenchymal stem/stromal cells (MSCs) have been demonstrated to hold great potential for the treatment of several diseases. Their therapeutic effects are largely mediated by paracrine factors including exosomes, which are nanometer-sized membrane-bound vesicles with functions as mediators of cell-cell communication. MSC-derived exosomes contain cytokines and growth factors, signaling lipids, mRNAs, and regulatory miRNAs. Increasing evidence suggests that MSC-derived exosomes might represent a novel cell-free therapy with compelling advantages over parent MSCs such as no risk of tumor formation and lower immunogenicity. This paper reviews the characteristics of MSC exosomes and their fate after in vivo administration, and highlights the therapeutic potential of MSC-derived exosomes in liver, kidney, cardiovascular and neurological disease. Particularly, we summarize the recent clinical trials performed to evaluate the safety and efficacy of MSC exosomes. Overall, this paper provides a general overview of MSC-exosomes as a new cell-free therapeutic paradigm.
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              Prostaglandin D2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia.

              Luis Garza, Yaping Liu, Zaixin Yang … (2012)
              Testosterone is necessary for the development of male pattern baldness, known as androgenetic alopecia (AGA); yet, the mechanisms for decreased hair growth in this disorder are unclear. We show that prostaglandin D(2) synthase (PTGDS) is elevated at the mRNA and protein levels in bald scalp compared to haired scalp of men with AGA. The product of PTGDS enzyme activity, prostaglandin D(2) (PGD(2)), is similarly elevated in bald scalp. During normal follicle cycling in mice, Ptgds and PGD(2) levels increase immediately preceding the regression phase, suggesting an inhibitory effect on hair growth. We show that PGD(2) inhibits hair growth in explanted human hair follicles and when applied topically to mice. Hair growth inhibition requires the PGD(2) receptor G protein (heterotrimeric guanine nucleotide)-coupled receptor 44 (GPR44), but not the PGD(2) receptor 1 (PTGDR). Furthermore, we find that a transgenic mouse, K14-Ptgs2, which targets prostaglandin-endoperoxide synthase 2 expression to the skin, demonstrates elevated levels of PGD(2) in the skin and develops alopecia, follicular miniaturization, and sebaceous gland hyperplasia, which are all hallmarks of human AGA. These results define PGD(2) as an inhibitor of hair growth in AGA and suggest the PGD(2)-GPR44 pathway as a potential target for treatment.
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                Author and article information

                Contributors
                Shivali Devjani: shivali.devjani@lahey.org
                Ogechi Ezemma: ogechi.ezemma@lahey.org
                Kristen J. Kelley: kristen.j.kelley@lahey.org
                Emma Stratton: emma.k.stratton@lahey.org
                Maryanne Senna:
                ORCID: http://orcid.org/0000-0002-7813-520X
                Maryanne.M.Senna@lahey.org
                Journal
                Journal ID (nlm-ta): Drugs
                Journal ID (iso-abbrev): Drugs
                Title: Drugs
                Publisher: Springer International Publishing (Cham )
                ISSN (Print): 0012-6667
                ISSN (Electronic): 1179-1950
                Publication date (Electronic): 11 May 2023
                Pages: 1-15
                Affiliations
                [1 ]GRID grid.415731.5, ISNI 0000 0001 0725 1353, Department of Dermatology, , Lahey Hospital and Medical Center, ; 67 South Bedford St, #100, Burlington, MA 01803 USA
                [2 ]GRID grid.38142.3c, ISNI 000000041936754X, Harvard Medical School, ; Boston, MA USA
                Author information
                http://orcid.org/0000-0002-7813-520X
                Article
                Publisher ID: 1880
                DOI: 10.1007/s40265-023-01880-x
                PMC ID: 10173235
                PubMed ID: 37166619
                SO-VID: 3e4a1bcd-648a-44e4-a448-d04ddaa67767
                Copyright © © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2023, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
                License:

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

                History
                Date accepted : 17 April 2023
                Categories
                Subject: Review Article

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