Androgenetic Alopecia: Disease-Characteristics Research Report

Scope. Androgenetic alopecia (AGA) is a common, complex, polygenic, androgen-dependent, non-scarring hair-loss disorder. “Male-pattern hair loss” (MPHL) and “female-pattern hair loss” (FPHL) denote its principal sex-patterned clinical presentations. Evidence below is disease-level and aggregated from publications and registries—not individual EHR data—unless a cohort is explicitly described.

Table: This table provides a compact, ontology-mapped summary of key disease characteristics for androgenetic alopecia, curated from clinical and genomic literature.

1. Disease information

AGA is characterized by progressive conversion of pigmented terminal scalp hairs into shorter, finer, often depigmented vellus-like hairs through repeated shortening of anagen and follicular miniaturization. Men usually develop bitemporal recession and frontal–mid-scalp–vertex loss, whereas women more often develop diffuse central/vertex thinning with relative preservation of the frontal hairline. Occipital/parietal follicles are comparatively resistant, especially in men. The condition is non-scarring: follicular ostia and potentially recoverable miniaturized follicles remain until advanced disease. (duran2024thebiologyand pages 6-7, souza2026useofgenetics pages 1-2)

Identifiers and synonyms. MONDO identifies androgenetic alopecia as MONDO:0005339; Open Targets also maps a historical “androgenetic alopecia 1” entity to MONDO:0007184. Common terms include androgenic alopecia, pattern hair loss, common baldness, male-pattern baldness/MPHL and female-pattern hair loss/FPHL. Common coding mappings include ICD-10-CM L64.9 (androgenic alopecia, unspecified), L64.0 (drug-induced androgenic alopecia), L64.8 (other androgenic alopecia), and MeSH Androgenetic Alopecia. Exact ICD-11 and SNOMED mappings should be terminology-server validated before ingestion because national extensions differ. (OpenTargets Search: androgenetic alopecia)

A concise 2024 review states: “Androgenetic alopecia is a highly prevalent condition mainly affecting men,” and emphasizes that it is related to aging and genetics while lifestyle and other factors may contribute. Publication: February 2024; DOI/URL: https://doi.org/10.3390/ijms25052542. (duran2024thebiologyand pages 11-13)

2. Etiology

Causal architecture

AGA is not ordinarily caused by one pathogenic mutation. It reflects age-dependent expression of polygenic susceptibility in androgen-responsive scalp follicles. Testosterone is converted to dihydrotestosterone (DHT) by 5α-reductases; DHT–AR signaling in susceptible dermal papilla cells changes paracrine support for epithelial progenitors and progressively shortens anagen. Female disease is more heterogeneous and can occur without measurable systemic androgen excess. (duran2024thebiologyand pages 6-7, souza2026useofgenetics pages 3-4)

Risk factors

• Genetic/familial: Twin and family data indicate strong heritability, often estimated near or above 80%. The AR/EDA2R X-chromosome region is the best-known signal, but numerous autosomal loci demonstrate polygenicity. Family history was associated with AGA presence (OR 2.72), progression (OR 4.24), and paternal history with presence (OR 2.22) in a meta-analysis of 31 studies, 11,224 cases and 36,825 controls searched through January 5, 2024. (duran2024thebiologyand pages 11-13, li2026riskfactorsfor pages 1-2)
• Age and sex: Clinically relevant AGA affects about 30% of men by age 30, nearly 50% by 50, and more than 70% in later decades. Female prevalence rises markedly after menopause; summarized estimates were 6% below age 50 and 30–40% above age 70. (duran2024thebiologyand pages 6-7, souza2026useofgenetics pages 1-2)
• Smoking/metabolic factors: Smoking was associated with presence (OR 1.46) and progression (OR 1.60); insulin resistance (SMD 0.40), fasting insulin (SMD 0.48), and male hypertension (OR 1.60) were associated with AGA. Alcohol, poor/insufficient sleep and overweight/obesity were linked mainly to progression. These observational associations do not establish causation and may be confounded. (li2026riskfactorsfor pages 1-2)
• Early-onset disease: A 2024 scoping review of 65 studies reported family history, smoking, unhealthy diet and high BMI as recurrent factors and examined associations with metabolic syndrome, insulin resistance, dyslipidemia and cardiovascular disease. Most studies were case-control and male-only, limiting causal and female inference. DOI: https://doi.org/10.1371/journal.pone.0299212.

Protective factors and gene–environment interaction

No genetic variant or lifestyle exposure is sufficiently validated as clinically actionable protection. Avoiding smoking and correcting documented nutritional deficiency are reasonable general-health measures, but evidence that either prevents genetically susceptible AGA is inadequate. The likely interaction is that inherited follicular androgen sensitivity sets vulnerability while age, endocrine milieu, smoking, metabolic dysfunction, inflammation and oxidative stress modify onset or progression; direct, replicated G×E estimates remain sparse. There is no infectious cause, zoonotic transmission or vaccine-preventable trigger.

3. Phenotypes

• Patterned non-scarring scalp alopecia: adult-onset, insidious, chronic and variably progressive. Men show temporal recession and vertex/frontal loss; women usually show widening of the central part and diffuse crown thinning. Suggested HPO: HP:0001596 Alopecia, HP:0011364 Thinning hair, HP:0002286 Premature baldness. (duran2024thebiologyand pages 6-7, souza2026useofgenetics pages 1-2)
• Follicular miniaturization: terminal-to-vellus transformation, reduced shaft diameter/density and increased single-hair follicular units. Suggested phenotype annotation: hair-shaft thinning/miniaturization; retain as a disease-specific clinical feature if no exact HPO term is available. (duran2024thebiologyand pages 6-7)
• Trichoscopic phenotype: A 2024 systematic review found hair-diameter variability in 94.07%, vellus hairs in 66.45%, and peripilar sign in 43.27% of patients. These are valuable indicators, particularly in women and early disease. Publication: March 2024; DOI: https://doi.org/10.3390/jcm13071962.
• Psychological burden: distress, body-image dissatisfaction, anxiety, depression and reduced self-esteem occur in subsets, especially younger or care-seeking patients. However, burden is heterogeneous: among 892 Finnish men aged 46, AGA prevalence was 68.5%—39.0% mild, 33.2% moderate and 27.8% severe—with no significant difference in measured anxiety, depression, self-esteem or overall QoL. Thus visible alopecia is not synonymous with psychiatric morbidity. DOI: https://doi.org/10.1136/bmjopen-2021-049855.

There are no defining laboratory abnormalities. Hyperandrogenism signs in women—irregular menses, acne, hirsutism or virilization—suggest an associated endocrine disorder rather than a required AGA phenotype.

4. Genetic and molecular information

Susceptibility genes—not Mendelian causal genes

GWAS had catalogued 119 significant variants across eight studies through 2021. The strongest summarized signal, rs200644307, lies approximately 500 kb from AR and may act through cis-regulation; its function is not established. Recurrently implicated regions/genes include AR/EDA2R, chromosome 20p11, SRD5A1, SRD5A2, CYP19A1, WNT10A, WNT6, RSPO2, LGR4, DKK2, FGF5, HDAC9, EBF1, PAX1, MAPT and others. Open Targets prioritizes SRD5A2, FGF5, SRD5A1/3, WNT10A, RSPO2, DKK2, AR and developmental transcription factors, but these disease–target associations do not mean that rare pathogenic variants in each gene cause ordinary AGA. (OpenTargets Search: androgenetic alopecia, duran2024thebiologyand pages 11-13, souza2026useofgenetics pages 3-4)

Accordingly, routine ClinVar-style “pathogenic/likely pathogenic” variant classification, carrier frequency, somatic mutation testing and germline mosaicism are generally not applicable to common AGA. Risk alleles are predominantly germline, common and small-effect; penetrance is incomplete, sex- and age-dependent, and expressivity variable. No consistent chromosomal aneuploidy, translocation, repeat expansion or mitochondrial mutation defines AGA.

Epigenetics and molecular profiling

Human balding-versus-nonbalding scalp studies report differential mRNA, miRNA and lncRNA expression involving WNT, HIF-1, Hippo, inflammatory, stress and fibrosis programs (reported transcriptomic PMIDs include 29122575 and 35862273). A 2024 TWAS identified 52, 75 and 144 expression–phenotype associations across increasingly severe MPB categories and 10, 11 and 54 putative causal genes after conditional analysis; these are computational prioritizations requiring functional validation. (duran2024thebiologyand pages 11-13)

Single-cell atlases demonstrate marked follicular heterogeneity—23 subpopulations in human anagen follicles from five transplant donors and dozens of epithelial/mesenchymal states in mouse skin—but AGA-specific, replicated single-cell and spatial maps remain limited. Epigenetic involvement is plausible through regulatory GWAS enrichment and loci such as HDAC9, but no methylation signature is validated diagnostically. (duran2024thebiologyand pages 11-13)

5. Environmental information

No toxin, radiation exposure, occupational agent or pathogen is accepted as a primary cause. Smoking, alcohol, poor sleep, diet, obesity and metabolic dysfunction have epidemiologic associations of varying consistency. Nutritional deficiencies can independently cause diffuse shedding and may coexist with AGA; indiscriminate supplements are not evidence-based in replete patients. Mechanical traction, chemotherapy, thyroid disease, severe illness and medications should instead prompt evaluation for alternative or superimposed alopecia. (li2026riskfactorsfor pages 1-2)

6. Mechanism/pathophysiology

Ordered causal chain

1. Polygenic susceptibility plus age and sex-hormone context leads to region-specific androgen sensitivity in scalp follicular dermal papilla cells.
2. 5α-reductase-mediated conversion of testosterone to DHT leads to high-affinity DHT binding and nuclear activation of AR in susceptible dermal papilla cells.
3. DHT–AR transcriptional signaling leads to altered paracrine output—including increased DKK1, IL-6, TGF-β-related/fibrotic and prostaglandin-D2 programs—and premature dermal-papilla senescence; the relative contribution of each branch is partly inferred from human scalp expression and in-vitro experiments.
4. DKK1 and related antagonism leads to suppression of WNT/β-catenin-dependent epithelial–mesenchymal signaling and impaired activation/support of follicular epithelial stem/progenitor cells.
5. Parallel PGD2–PTGDR2 signaling leads to reduced shaft elongation and promotion of catagen, while inflammatory, oxidative-stress and perifollicular-remodeling branches likely amplify dysfunction.
6. Reduced growth signaling and premature catagen lead to shortened anagen, relatively increased telogen, smaller dermal papillae and progressive terminal-follicle miniaturization.
7. Repeated miniaturizing cycles result in thin, short, depigmented vellus-like hairs and the clinically visible male or female pattern of non-scarring scalp alopecia. (duran2024thebiologyand pages 6-7, souza2026useofgenetics pages 3-4)

Cells, processes and ontology suggestions

Primary cells are dermal papilla fibroblasts (CL:0002551), hair-follicle stem/progenitor keratinocytes, matrix keratinocytes, dermal sheath fibroblasts, endothelial cells and perifollicular immune cells. Suggested GO biological processes include steroid-hormone-mediated signaling (GO:0043401), WNT signaling (GO:0016055), hair-follicle development, hair cycle, cell senescence, regulation of apoptosis, inflammatory response, extracellular-matrix organization and angiogenesis. Relevant compartments include nucleus/AR transcriptional complex, cytosol, plasma membrane and extracellular matrix.

This mechanism is principally altered signaling rather than protein misfolding or enzyme deficiency. DHT itself is not necessarily systemically elevated; local enzyme activity and follicular receptor sensitivity matter. Open Targets’ highest disease association was SRD5A2, consistent with the clinical validation of 5α-reductase inhibition. (OpenTargets Search: androgenetic alopecia)

7. Anatomical structures affected

The primary organ is skin of the scalp and its pilosebaceous units; the directly affected mini-organ is the hair follicle (UBERON:0002073). In men the frontal, temporal, mid-scalp and vertex follicles are preferentially affected, with relative occipital/parietal sparing; female involvement is typically central/vertex and more diffuse. Distribution is bilateral and broadly symmetric, not lateralized. (duran2024thebiologyand pages 6-7, souza2026useofgenetics pages 1-2)

At tissue level, affected structures include follicular epithelium, connective-tissue dermal papilla/sheath, perifollicular extracellular matrix and microvasculature. There is no obligatory secondary-organ injury. Endocrine/metabolic comorbidities are associations, not anatomical spread.

8. Temporal development

Onset is commonly post-pubertal and insidious; men tend to present earlier than women. Early disease manifests as reduced density, hair-diameter diversity and increased vellus/single-hair units; intermediate disease produces evident patterned thinning; advanced disease shows extensive miniaturization. The course is chronic, slowly progressive and highly variable. Spontaneous durable remission is uncommon, while treatment can stabilize or partially reverse miniaturization. Benefits generally diminish after treatment withdrawal. Earlier intervention is biologically favored because miniaturized follicles are more recoverable than long-standing severely involuted units. (duran2024thebiologyand pages 6-7, souza2026useofgenetics pages 1-2)

9. Inheritance and population

Inheritance is multifactorial/polygenic, not simple autosomal dominant or X-linked, despite strong X-chromosomal AR/EDA2R effects. Penetrance is incomplete and age/sex dependent; expressivity varies in onset, distribution and severity. Anticipation, carrier status, consanguinity and classic founder mutations are not established features. (duran2024thebiologyand pages 11-13, souza2026useofgenetics pages 3-4)

Prevalence depends strongly on age, ancestry, case definition and ascertainment. Up to 50% of men and 40% of women may be affected by midlife in some reviews; Caucasian men have historically shown the highest reported prevalence, while onset/severity vary across ancestries. In 9,227 dermatologist-examined Chinese university freshmen, prevalence was 5.3/1,000, including 7.9/1,000 males; female sex had OR 0.29. The young age explains why these values are far below lifetime estimates. DOI: https://doi.org/10.1371/journal.pone.0263912. (kumaresan2025adecadeof pages 1-2, souza2026useofgenetics pages 1-2)

Reliable annual incidence per 100,000 is not established globally. Apparent healthcare prevalence also reflects access, cosmetic concern and coding behavior.

10. Diagnostics

Diagnosis is primarily clinical: compatible patterned non-scarring thinning, preserved follicular openings, gradual onset and family history. Grade men with Hamilton–Norwood and women with Ludwig/Sinclair; BASP can describe either sex. Serial standardized photography or phototrichograms support monitoring. Trichoscopy should assess shaft-diameter variability, miniaturized/vellus hairs, peripilar sign, yellow dots and increasing single-hair follicular units. (duran2024thebiologyand pages 6-7, khare2023dermoscopyofhair pages 1-2)

Laboratory tests are selective, not confirmatory. In women with diffuse shedding, menstrual/endocrine symptoms or systemic signs, consider CBC/ferritin, TSH and targeted androgen testing; evaluate nutritional deficiency based on history. Scalp biopsy is reserved for uncertainty: horizontal sections typically show reduced terminal:vellus ratio, increased miniaturized follicles, altered anagen:telogen ratio and sometimes mild perifollicular inflammation/fibrosis.

Differential diagnosis: telogen effluvium (diffuse shedding without patterned miniaturization), alopecia areata (patches, exclamation-mark/black-dot/tapering-hair pattern), traction alopecia (hairstyle distribution), trichotillomania (broken hairs of variable length), tinea capitis (scale/infection), frontal fibrosing alopecia or lichen planopilaris (loss of ostia and inflammatory scarring), central centrifugal cicatricial alopecia, thyroid/nutritional disease and medication-induced shedding.

Routine WES, WGS, panels, AR testing, CMA, karyotype, FISH, mtDNA or repeat-expansion testing has no validated diagnostic role. Polygenic scores, transcriptomics, proteomics and liquid biopsy remain research tools.

11. Outcome and prognosis

AGA is medically benign and does not reduce survival or life expectancy. Morbidity is cosmetic and psychosocial rather than organ failure or mortality. Untreated disease commonly progresses, but at an unpredictable rate; existing follicles can be stabilized or thickened, whereas drugs do not generate an unlimited supply of new follicles. Surgical redistribution can provide durable cosmetic coverage but donor hair is finite. (britva2026regenerativestrategiesfor pages 19-19)

QoL impact should be measured rather than assumed, using DLQI, EQ-5D, SF-36/PROMIS or hair-specific instruments. Younger age, female sex in some settings, rapid progression, severe visible loss and body-image concern may predict greater distress, but population evidence is inconsistent. (kumaresan2025adecadeof pages 1-2)

12. Treatment

Practical strategy

1. Confirm AGA and exclude scarring or superimposed shedding.
2. Offer topical minoxidil to either sex; discuss initial shedding, irritation and lifelong maintenance.
3. For men, add oral finasteride after sexual, fertility and psychiatric counseling; consider dutasteride off-label where appropriate.
4. For selected women, consider low-dose oral minoxidil and antiandrogen therapy after cardiovascular, pregnancy and endocrine assessment.
5. Use PRP, microneedling or cleared low-level-light devices as adjuncts when expectations and evidence uncertainty are discussed.
6. Consider transplantation for stable, advanced disease with adequate donor density; continue medical treatment to protect non-transplanted hair.

Pharmacotherapy and outcomes

• Topical minoxidil 2–5%—FDA-approved; prolongs anagen and requires continuous use. Reviews report moderate regrowth in approximately 30–40%. Adverse effects include irritation, unwanted facial/body hypertrichosis and transient initial shedding. Suggested NCIt: minoxidil (C62024). (burshtein2026emergingpharmacotherapiesand pages 2-3, kumaresan2025adecadeof pages 6-8)
• Low-dose oral minoxidil, approximately 0.25–5 mg/day—off-label. Useful when topical therapy is poorly tolerated, but hypertrichosis, edema, tachycardia, hypotension and rare serious cardiovascular effects require screening and monitoring. (kumaresan2025adecadeof pages 6-8)
• Finasteride 1 mg/day—FDA-approved for male AGA; inhibits type-II 5α-reductase. Sexual adverse effects were approximately 2–4% in reviewed male studies; regulators also warn about mood/psychiatric and potentially persistent sexual symptoms. It is contraindicated in pregnancy; crushed/broken tablets should not be handled by someone who is or may be pregnant. Suggested NCIt: finasteride (C1265). (burshtein2026emergingpharmacotherapiesand pages 2-3, gupta2025relativeefficacyof pages 6-6)
• Dutasteride 0.5 mg/day—dual type-I/II inhibitor, off-label in the US but approved for AGA in some countries including Japan and South Korea. It generally produces greater hair-count improvement than finasteride 1 mg, with similar overall tolerability but concern for sexual and psychiatric adverse effects. Suggested NCIt: dutasteride (C47491). (burshtein2026emergingpharmacotherapiesand pages 2-3)
• Women: spironolactone and, less commonly, finasteride/dutasteride in carefully selected patients are off-label. Antiandrogens require reliable contraception and monitoring appropriate to drug and comorbidity. Evidence is less standardized than in men.

A large randomized Chinese study reported improvement at 12 months in 80.5% with finasteride, 59% with 5% topical minoxidil and 94.1% with their combination. Combination series/reviews report hair-density improvements of roughly 18–32%, versus 8–15% with monotherapy, although protocols and endpoints vary. (burshtein2026emergingpharmacotherapiesand pages 2-3, kumaresan2025adecadeof pages 11-12)

Procedural and surgical treatments

PRP can improve density and shaft thickness, but preparation, dosing and endpoints are heterogeneous; benefit commonly lasts 3–6 months and maintenance is needed. One double-blind split-scalp trial of 35 participants found no superiority to placebo, illustrating uncertainty. Microneedling may activate wound/WNT programs and enhance topical delivery; 12–24-week trials generally favored combination with minoxidil over minoxidil alone. LLLT/photobiomodulation devices have modest efficacy and favorable short-term tolerability. Hair transplantation by follicular-unit excision or strip harvesting redistributes androgen-resistant donor follicles and is the principal durable structural intervention; risks include scarring, shock loss, poor growth, unnatural design and depletion of donor supply. (britva2026regenerativestrategiesfor pages 19-19, kumaresan2025adecadeof pages 6-8)

Emerging therapeutics and trials

Topical AR antagonists such as pyrilutamide/KX-826, topical finasteride/dutasteride carriers, AR-silencing RNA, prostaglandin modulators, WNT-directed approaches, exosomes, conditioned media, adipose/dermal-sheath cells and follicle organoids are investigational. Exosome products remain poorly standardized/unregulated, and long-term safety is unknown. (souza2026useofgenetics pages 3-4, britva2026regenerativestrategiesfor pages 19-19, kumaresan2025adecadeof pages 1-2)

Current registry examples include phase-3 oral-minoxidil studies in women (NCT05888922, planned n=520) and men (NCT07529977, planned n=372), multiple VDPHL01 phase 2/3 programs (NCT06527365, NCT06724614, NCT06972264, NCT07146022), and a mechanistic topical-minoxidil/JAK2 study (NCT07563036, n=25). Registry status and enrollment should be rechecked at https://clinicaltrials.gov before database release; NCT07563036 had no outcome results in the retrieved record. (NCT07563036 chunk 2)

There is no established genotype-guided prescribing algorithm. SULT1A1 activity is a candidate minoxidil-response biomarker: one small study reported regrowth in 75% with a SULT1A1 adjuvant versus 33% with placebo adjuvant over 60 days, but this is not routine pharmacogenomics. (gupta2025relativeefficacyof pages 6-6)

13. Prevention

No proven primary prevention, vaccine, prophylactic medication or population screening program exists. Modifiable-risk counseling—avoid smoking, treat metabolic disease, maintain adequate nutrition and avoid traction—supports general/follicular health but is not proven to override inherited risk. Secondary prevention consists of early clinical/trichoscopic detection and prompt therapy to preserve miniaturizing follicles. Tertiary prevention includes adherence, serial monitoring, managing adverse effects and psychosocial support. Genetic carrier, prenatal or preimplantation screening is inappropriate for ordinary polygenic AGA.

14. Other species and natural disease

A directly homologous, common spontaneous veterinary disorder with the same human scalp distribution is not firmly established. Mammals share AR, steroid metabolism and WNT-regulated follicle cycling, but coat-hair biology and synchronized cycles differ substantially. “Pattern alopecia” in dogs is phenotypically relevant but should not automatically be equated with human polygenic AGA. There is no infectious transmission, zoonotic potential or cross-species contagion.

15. Model organisms and experimental systems

• Human in vitro: primary dermal papilla cells from balding/nonbalding scalp are exposed to DHT or pathway modulators to study AR, DKK1, senescence and growth signaling. Two-dimensional culture is scalable but rapidly loses papilla inductivity and lacks epithelial–mesenchymal architecture.
• Human ex vivo: isolated scalp follicles or punch/excision explants preserve native cycling and regional identity for short-term drug testing but are scarce, variable and short-lived.
• Mouse (Mus musculus; NCBI Taxon 10090): DHT-treated C57BL/6 models test hair-growth inhibition and 5α-reductase/WNT interventions. Mouse follicles cycle synchronously, have different androgen responses and do not reproduce human patterned scalp loss.
• Stump-tailed macaque (Macaca arctoides; NCBI Taxon 9540): develops androgen-responsive frontal balding and has historically been useful for 5α-reductase inhibitors, but expense, ethics and limited access constrain use.
• 3D spheroids, microfollicles and skin/hair-bearing organoids: improve papilla inductivity and multicellular organization and may support regenerative/transplantation research. A systematic appraisal found 70/101 AGA model studies used mainly 2D in-vitro systems, 27 used mice or monkeys, only four used human explants, and none then used 3D organoids/organotypic AGA skin—highlighting a translational gap. A 2024 review emphasizes that fully recreating diverse follicular cell organization and durable cycling remains difficult. DOI: https://doi.org/10.1002/ski2.15 and https://doi.org/10.3390/biology13050312. (liu2026developmentandvalidation pages 13-13)

Evidence appraisal and knowledge gaps

The strongest causal evidence combines human genetics, regional human scalp biology and therapeutic validation of SRD5A inhibition. Evidence for smoking/metabolic factors remains observational; immune, oxidative, epigenetic and many omics pathways are biologically plausible but not yet validated as independent clinical targets. Treatment evidence is strongest for minoxidil and finasteride, moderate for dutasteride and several adjunctive devices/procedures, and preliminary for topical AR antagonists, RNA, cells, exosomes and organoids. Major needs are ancestry-diverse longitudinal cohorts, standardized female phenotyping, AGA-specific single-cell/spatial atlases, validated response biomarkers and long-term head-to-head safety trials. (OpenTargets Search: androgenetic alopecia, duran2024thebiologyand pages 11-13, li2026riskfactorsfor pages 1-2, burshtein2026emergingpharmacotherapiesand pages 2-3)

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13. (liu2026developmentandvalidation pages 13-13): Shizhao Liu, Wenzhen Li, Botian Jiang, Haoyang Li, Jian Chen, Zhe-Xiang Fan, Zhiqi Hu, Qian Qu, and Yong Miao. Development and validation of a comprehensive in vitro organ model for androgenetic alopecia. Jun 2026. URL: https://doi.org/10.1186/s12896-026-01176-4, doi:10.1186/s12896-026-01176-4. This article has 1 citations and is from a peer-reviewed journal.

14. (li2026riskfactorsfor pages 1-2): Haoyang Li, Wenzhen Li, Jiaxian Zhang, Qihong Liang, Yingjie Zhao, Zehong Guo, Botian Jiang, Zhan Wang, Qian Qu, Shengli An, and Yong Miao. Risk factors for androgenetic alopecia: a systematic review and meta-analysis. BMC Public Health, Jan 2026. URL: https://doi.org/10.1186/s12889-026-26258-y, doi:10.1186/s12889-026-26258-y. This article has 3 citations and is from a peer-reviewed journal.

15. (kumaresan2025adecadeof pages 6-8): Subalakshmi Kumaresan, Dhivya Palaniappan, Navakumar Manickam, Seethalakshmi Ganga Vellaisamy, and Kannan Gopalan. A decade of progress in androgenetic alopecia management: emerging therapies and multimodal strategies. IP Indian Journal of Clinical and Experimental Dermatology, 11(4):457-472, Dec 2025. URL: https://doi.org/10.18231/j.ijced.13629.1765276898, doi:10.18231/j.ijced.13629.1765276898. This article has 0 citations.

16. (gupta2025relativeefficacyof pages 6-6): Aditya K. Gupta, Mary A. Bamimore, and Mesbah Talukder. Relative efficacy of conventional monotherapies and select nonconventional, over‐the‐counter products for male androgenetic alopecia: a network meta‐analysis study. Journal of Cosmetic Dermatology, Oct 2025. URL: https://doi.org/10.1111/jocd.70483, doi:10.1111/jocd.70483. This article has 3 citations and is from a peer-reviewed journal.

17. (kumaresan2025adecadeof pages 11-12): Subalakshmi Kumaresan, Dhivya Palaniappan, Navakumar Manickam, Seethalakshmi Ganga Vellaisamy, and Kannan Gopalan. A decade of progress in androgenetic alopecia management: emerging therapies and multimodal strategies. IP Indian Journal of Clinical and Experimental Dermatology, 11(4):457-472, Dec 2025. URL: https://doi.org/10.18231/j.ijced.13629.1765276898, doi:10.18231/j.ijced.13629.1765276898. This article has 0 citations.

18. (NCT07563036 chunk 2): heba ahmed abdelgayed ibrahim. JAK2 Expression in Androgenetic Alopecia Before and After Topical Minoxidil. Kasr El Aini Hospital. 2026. ClinicalTrials.gov Identifier: NCT07563036

Artifacts

• Edison artifact artifact-00

Reference Validation

Checked with linkml-reference-validator 0.2.1.

All extracted references resolved successfully.

Term Validation

Checked with linkml-term-validator 0.4.5, through the ols: adapter.

Every term resolved, and every label the report gave matched.