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This study identified histologic lesions and a defect in adhesion molecules causing hair loss in mice with the bal mutation, linked to a mutation in the desmoglein 3 gene.

This study found that non-balding dermal papilla cells emphasized extracellular matrix organization and reduced inflammation when cultured in 3D or with adipose-derived stem cells, unlike balding cells which maintained inflammatory pathways.

This study found that co-culturing dermal papilla cells in a 3D structure with adipose-derived stem cells may enhance the expression of hair inductivity markers compared to 2D cultures.

The Celsr1 gene is crucial for normal hair patterning in mice.

This study found that dermal papilla cells from balding follicles exhibit distinct growth characteristics compared to non-balding cells, suggesting their potential as a model for understanding androgenetic alopecia.

This study found that balding dermal papilla cells show premature senescence and altered expression of stress and DNA damage markers, suggesting sensitivity to environmental stress in androgenetic alopecia.

This study suggests that alkaline phosphatase-regulated expression of CCL5 contributes to the trichogenicity of human dermal papilla spheres.

This study found that dermal papilla cells from balding scalp hair follicles have significantly higher levels of androgen receptors than those from non-balding follicles, supporting their in vivo androgen response.

This study found that Celsr1, not Celsr2, is the primary protein involved in establishing planar cell polarity and hair follicle polarization in the epidermis of mice.

In this study, researchers identified a mutation in mice that causes hair loss and immune system issues, located on chromosome 18.

This study suggests that down-regulation of vasculature-related genes in dermal papilla cells from balding scalps might contribute to the development of androgenetic alopecia.

In this study, researchers found that the gene LRRC15 was overexpressed in dermal papilla cells from balding areas compared to non-balding areas in patients with androgenetic alopecia.

This study found that ILC1-like cells can induce alopecia areata in healthy human hair follicles, challenging the traditional belief that the disease is primarily driven by CD8+ T cells.

In this study using mice, simultaneous deficiencies in claudin-1 and claudin-3 were associated with hair loss and altered hair follicle architecture during the telogen phase, suggesting a role in hair retention.

In this study, baricitinib was evaluated for its effectiveness in promoting concurrent regrowth of scalp hair, eyebrows, and eyelashes in patients with severe alopecia areata, showing clinically meaningful responses compared to placebo.

EBF1 controls hair type and length.

This study identified proteins that are differentially expressed in balding versus non-balding dermal papilla cells, potentially aiding the understanding and treatment of androgenetic alopecia.

Hair shaft changes may be linked to CCCA, but their role is unclear.

This study mapped the curly mutation in mice to a specific region on chromosome 11, identifying it as a candidate model for studying human genetic hair disorders.

This study found that mutant mice with the we/we wal/wal genotype exhibit significant defects in hair shaft structure and epidermis stratification, correlating with postnatal alopecia symptoms.

This study found that B6.CD80CD86−/− mice developed autoimmune-like alopecia with nearly 100% incidence by 40 weeks, making them a promising model for studying human alopecia areata.

In this study, researchers successfully established immortalized human frontal and occipital scalp dermal papilla cell lines from androgenetic alopecia patients, observing distinct gene expression, androgen receptor levels, and hair follicle growth effects between these regions, which may help advance hair loss research and therapeutic development.

This study found that the mitotic arrest deficient protein MAD2B negatively affects TCF4-induced growth and proliferation of dermal papilla cells, which are vital for hair follicle development.

In vivo using the C3H mouse model, this study observed that BST2 expression occurs before hair loss in alopecia areata and is followed by an increase in epidermal γδ T cell numbers.

This study found that plasmacytoid dendritic cells may initiate alopecia areata in mice by overexpressing interferon-alpha.

This study found that allergen treatment in alopecia areata mice appeared to alter leukocyte subset distribution and impaired dendritic cell migration, which may affect T-cell activation and hair follicle recovery.