Androgenetic alopecia (AGA), the most common cause of hair loss, is influenced by various risk factors. Metabolic syndrome constitutes a collection of risk factors elevating the risk of cardiovascular disease. The presence of early-onset AGA could serve as an indicator of the emergence of metabolic syndrome, yet to date, no research has examined these parameters in AGA. This is a cross-sectional study comparing two groups; early onset versus normal onset AGA. Forty participants were enlisted and evenly distributed into the two groups. Subsequently, participants underwent examinations utilizing trichoscopy, trichoscan, and laboratory assessments. Apart from waist circumference, BMI, and age of alopecia onset, there were no notable differences concerning sociodemographic and clinical features. In terms of hair growth parameters, the telogen hair rate stands out as the sole indicator exhibiting a significant difference between both groups, while trichoscopy data also revealed varying hair characteristics. Lastly, metabolic parameters namely triglyceride, fasting blood glucose, HbA1c and HDL differ significantly, with the normal onset group demonstrating a higher prevalence of metabolic abnormality. This suggests a potential association between AGA and metabolic syndrome. However, the exact nature of this relationship remains uncertain, necessitating further research with larger samples, specific age groups and diverse study designs.

Androgenic alopecia (AGA) and alopecia areata (AA) are two highly prevalent conditions, affecting both men and women of a wide range of ages, which strongly impact their quality of life and self-esteem. Both pathologies are deemed to be reversible, although conventional therapies have shown limited scope and efficacy. New therapeutic approaches, focusing on the degenerative changes that take place in the hair follicle, are needed to achieve better outcomes. For instance, adipose-derived stem cells (ADSC), abundant and easy to obtain, hold great potential in follicular regeneration. ADSCs can be isolated as stromal vascular fraction (SVF) by the enzymatic digestion of the lipoaspirate or as nanofat by the mechanical breakdown of adipocytes. In addition, commercial preparations of the conditioned medium of the ADSCs secretome (ADSC-conditionate medium [CM]) have entered the market as an appealing alternative because of their comparatively lower cost and accessibility. A search was conducted, crossing relevant terms, on PubMed Central and Google Scholar. Criteria for inclusion were studies in the past 10 years on humans with AGA or AA, where either SVF, nanofat, or ADSC-CM was tested as the main treatment. Eleven publications qualified: two studied nanofat, three, ADSC-CM, and six, SVF, either individually or in combination with other therapies. Only one randomized controlled trial (RCT) was found and classified as evidence 2b according to the Sackett scale. The rest were case-control studies or case series with small samples and no control, graded as evidence 3b and 4. A meta-analysis could not be conducted due to the heterogenicity of the study designs. Given the evidence obtained, Level D NICE recommendation was established. However, we consider that the positive findings are sufficiently consistent to support the elaboration of further RCTs that share criteria and methods.

BACKGROUND: Although several studies report on the suppressing effects of estrogen therapy on facial and body hair in transgender and nonbinary (TGNB) individuals, few studies have elucidated its effects on hairline stability on the scalp. In this study, we assessed the influence of estrogen therapy on forehead length.
METHODS: All TGNB patients, aged 30 years or older, assigned male at birth (AMAB) seeking facial feminization surgery were included in the study. Central and forehead lengths were collected at the initial consultation visits. Variables, including age, duration of hormone replacement therapy (HRT), presence of spironolactone, and presence of other hair treatments, such as finasteride, dutasteride, or minoxidil, that potentially influence hair growth were collected by chart review. Multivariable linear regressions were constructed with relevant predictor variables while also incorporating global health scores as a proxy for psychological effects on hair loss.
RESULTS: Overall, 171 patients were included in this study, with a median age of 36.0 (interquartile range (IQR) 32.0-46.0) years and median HRT duration of 2.0 (IQR 1.0-6.0) years. Multivariable linear regressions revealed no significant predictors for central forehead length. However, lateral forehead length was positively predicted by age (B=0.06, 95% confidence interval (CI) [0.03-0.08], p < 0.001) and hair treatment (B=0.66, 95% CI [0.14-1.18], p = 0.01), but negatively predicted by HRT duration (B=-0.07, 95% CI [-0.10 to -0.04], p < 0.001).
CONCLUSIONS: Although older age is a predictor of lateral hairline recession in TGNB AMAB individuals, lateral forehead length was also predicted to decrease by 0.07 cm with each year of feminizing hormone therapy in patients over 30 years of age.

Androgenic alopecia (AGA) typically manifests post-puberty, resulting in decreases in hair density, disruptions in the hair growth cycle, and alterations in hair follicle micro structure. Dihydrotestosterone (DHT) is a key hormone implicated in hair loss, especially on male. In this study, we found that each of arginine (Arg), arterial extract (AE) or biotin tripeptide-1 (BT-1), when combined with low level light therapy (LLLT, at 630 nm, 2 J/cm2), showed the efficacy in enhancing mitochondrial functions, cell proliferation and collagen synthesis in fibroblasts. Additionally, CARRIPOWER (the complexes of AE, BT-1, Arg, and Diaminopyrimidine derivatives), in conjunction with LLLT (630 nm, 2 J/cm2), showed promising results in dermal papilla cells (DPCs). The promising results contained not also inflammatory cytokines (IL-1β and IL-6) and cell pro apoptotic factor (TGF-β2) reduction, but also Wnt pathway inhibition by decreasing DKK1 level, and pro-hair growth factors (vascular endothelial growth factor (VEGF) and β-catenin) increase. This innovative combination therapy offers a potential solution for the treatment of AGA, addressing both hormonal and cellular factors involved in hair loss.

BACKGROUND: Increasing studies have reported a causal relationship between androgenetic alopecia (AGA) and lipid-related metabolites. However, the relationships between HDL-C, LDL-C, Omega-6, and Omega-3 with AGA remain unclear. Some research findings are even contradictory. Therefore, we designed this study to explore this issue.
METHODS: In this study, we selected seven exposure factors, screened SNPs with significant associations, removed linkage disequilibrium and weak instrumental variables, and conducted bidirectional MR analysis.
RESULTS: The study found that omega-6 and LDL-C, especially total cholesterol in medium LDL and total cholesterol in small LDL, are risk factors for the occurrence of androgenetic alopecia.
CONCLUSIONS: In summary, we found that various lipid-related metabolites have a causal relationship with the occurrence of androgenetic alopecia, providing new insights into the pathogenesis of androgenetic alopecia and offering references for clinical treatment of androgenetic alopecia.

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Androgenetic alopecia (AGA) is defined as the alopecia induced by androgens in genetically predisposed individuals. AGA results in progressive miniaturization of the hair follicles leading to vellus transformation of terminal hair. The high prevalence and wide range of expressed phenotypes in AGA is a result of a polygenic inheritance mode. The androgen receptor (AR) gene located on the X chromosome at Xq11-12 is the first gene to show genetic association with AGA. Newer genetic associations with AGA are under study. In early-onset AGA, obesity, diabetes, hypertension, dyslipidaemia, insulin resistance, benign prostatic hyperplasia (BPH), prostate cancers and coronary artery disease (CAD) are associated with AGA. Screening of early-onset AGA patients and intervention for metabolic syndrome and insulin resistance can prevent the development of cardiovascular disease (CVD) at an early stage. As effective treatments continue to be topical minoxidil, systemic finasteride and hair transplantations, newer modalities are under investigation. Understanding the genetic factors involved in AGA and continued research into newer therapies, such as cell-based therapies, will lead to effective treatment and improve the quality of life in patients with AGA.

Androgenic alopecia (AGA) is the most common type of alopecia and its treatments involve drugs that have various adverse effects and are not completely effective. Radiofrequency-based therapies (RF) are an alternative for AGA treatment. Although there is increasing clinical evidence of the effectiveness of RF for alopecia, its effects at the tissue and cellular level have not been studied in detail. The objective of this study was to analyze ex vivo the potential effect of RF currents used in capacitive resistive electrical transfer (CRET) therapy on AGA. Hair follicles (HFs) were donated by patients with AGA and treated with CRET. AGA-HFs were exposed in vitro to intermittent 448 kHz electric current in subthermal conditions. Cell proliferation (Ki67), apoptosis (TUNEL assay), differentiation (β-catenin), integrity (collagen and MMP9), thickness of the epidermis surrounding HF, proportion of bulge cells and melanoblasts in AGA-HF were analyzed by immunohistochemistry. CRET increased proliferation and decreased death of different populations of AGA-HF cells. In addition, the melanoblasts increased in bulge and the epidermis surrounding the hair follicle thickened. These results support the effectiveness of RF-based therapies for the treatment of alopecia. However, clinical trials are necessary to know the true effectiveness of CRET therapy and other RF therapies for AGA treatment.

In mice, hair growth follows a mosaic or wavy patterning. Therefore, synchronization of the hair growth cycle is required to adequately evaluate any trichogenic interventions pre-clinically. Depilation is the established method for synchronizing the growth phase of mouse hair follicles. When attempting to reproduce procedures reported in the literature, C57BL/6J mice developed severe wounds. This led us not only to optimize the procedure, but also to test the procedure in other strains, namely Sv129 and the F1 generation from C57BL/6J crossed with Sv129 (B6129F1 mixed background), for which the hair growth cycle has not been ascertained yet. Here, we describe an optimized depilation procedure, using cold wax and an extra step to protect the animal skin that minimizes injury, improving experimental conditions and animal welfare in all strains. Moreover, our results show that, although hair cycle kinetics are similar in all the analyzed strains, Sv129 and B6129F1 skins are morphologically different from C57BL/6J skin, presenting an increased number and size of hair follicles in anagen, consistent to the higher hair density observed macroscopically. Altogether, the results disclose an optimized mouse depilation method that excludes the detrimental and confounding effects of skin injury in hair growth studies and reveals the hair cycle features of other mouse strains, supporting their use in hair growth pre-clinical studies.

BACKGROUND: Alopecia affects patients\' appearance and psychology. Mixed-lineage kinase domain-like pseudokinase (MLKL)-mediated necroptosis plays a role in various skin diseases, but its effect on hair growth is unclear.
OBJECTIVE: To investigate the effects of MLKL on hair growth and its regulatory mechanisms and to determine the potential clinical value of Necrosulfonamide (NSA, a MLKL-targeting inhibitor) in promoting hair growth and counteracting dihydrotestosterone (DHT) inhibition of hair growth.
METHODS: The expression level of MLKL was detected in the scalp of androgenetic alopecia (AGA) patients and the skin tissues of mice. Knock down MLKL expression or use NSA to observe hair growth in vivo and in vitro.
RESULTS: In AGA patients, MLKL expression is elevated in the alopecia areas. In mice, MLKL is significantly expressed in the outer root sheath (ORS) cells of hair follicles, peaking during the catagen phase. Knockdown expression of MLKL in mice skin promoted hair growth. NSA enhanced hair growth and prevented hair follicle regression via the Wnt signaling. Reduced MLKL boosts ORS cell proliferation without directly impacting DPCs\' growth. Interestingly, NSA boosts DPCs\' proliferation and induction when co-cultured with ORS cells. Besides, NSA alleviated the inhibition of DHT on hair growth in vivo and vitro.
CONCLUSIONS: NSA inhibited the activation of MLKL in ORS cells, promoted the activation of Wnt signal in DPC cells, and improved the inhibition of hair growth by DHT, illuminating a new alopecia mechanism and aiding anti-alopecia drug development.