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In this study, researchers found that YAP and TAZ, when localized in the nucleus of basal layer cells, are crucial for skin regeneration and hair growth, with their loss leading to slower cell proliferation, hair loss, and impaired wound healing in mice.

This review examines integrins as pharmacological targets, discussing current integrin-based therapies and emphasizing the need to understand integrin mechanisms for successful drug development, without reporting new clinical results.

This study found that α3β1-integrin is crucial for maintaining normal hair follicle morphology in mice, as its deficiency leads to severe abnormalities despite not affecting interfollicular epidermal differentiation.

In this study, PINCH-1 gene loss in mouse epidermis led to detachment from the basement membrane, thickened skin, and hair loss, with findings suggesting PINCH-1 plays a role in keratinocyte adhesion through both ILK and EPLIN pathways.

In this study, gene inactivation in mouse hair follicle stem cells lacking ILK impaired wound healing by reducing their progeny’s contribution to the regenerating epidermis, but did not affect hair follicle regeneration.

Mutations in β1 integrins cause embryonic death but have milder effects on skin.

This study found that keratinocyte stem/progenitor cell-conditioned medium significantly enhanced hair growth in mice and increased the proliferation of human hair follicle cells.

In this study, researchers found that miR-3606-3p is significantly downregulated in skin fibrosis and correlates with disease severity, with its ability to inhibit key signaling pathways suggesting potential therapeutic applications for conditions like systemic sclerosis and keloids.

In this study, targeted inactivation of the integrin-linked kinase gene in melanoblasts led to defects in cell migration, proliferation, and ability to populate the skin, implicating an integrin-linked kinase-Rac1 connection in melanocyte function.

The study suggests that integrin β1 is crucial for maintaining liver microstructure and its absence may promote fibrosis by disrupting hepatocyte-extracellular matrix interactions and increasing TGF-β secretion.

This study found that integrin-linked kinase is crucial for various epidermal functions, including differentiation and barrier formation, and also plays a previously unreported role in melanocyte development and function.

This study found that absence of α3 integrin in mice led to faster wound healing but also caused inflammation, hair loss, and skin defects, suggesting complex roles in skin integrity and repair.

This study found that mice lacking CD61 had significantly shorter lower incisors compared to wild-type mice, suggesting CD61 is crucial for proper tooth growth and pre-ameloblast proliferation.

This study reported that the use of composite RGDmix hydrogel improved the survival and proliferation of human amniotic mesenchymal stem cells and increased growth factor expression, enhancing wound healing through the RGDSP/integrin αv/PI3K/AKT signaling pathway.

This study used single-cell techniques and lineage tracing to reveal that integrin α6 expression in neural crest cells can differentiate them into Schwann cells, melanocytes, and fibroblasts in skin, identifying integrin α6 as a potential marker for these derivatives.

This study found that epidermal-specific deletion of integrin α3β1 significantly reduces papilloma formation in a skin carcinogenesis model by modulating HB stem cell behavior and CCN2 expression.

The researchers concluded that blocking α1-integrin altered adhesion and enhanced migration in adult fibroblasts, suggesting its potential as a target for therapies aimed at reducing fibrosis.

This study found that knocking out the integrin β1 subunit in induced pluripotent stem cells enhanced their migration and improved their wound-healing effects in a mouse model.

This study found that stress-induced inactivation of the enzyme Dicer in melanocytes can cause premature hair greying by preventing proper melanocyte placement and melanin transfer in mice, suggesting the Dicer-miR92b-ItgaV pathway as an important link between stress and grey hair.

This study demonstrated that a keratin gel promotes nerve regeneration across critical defects in rabbit models, showing improved nerve conduction and muscle action potential compared to control treatments.

This study found that angiopoietin-1 significantly reduces apoptosis and promotes proliferation in human follicle dermal papilla cells under DHT-induced stress, suggesting its potential as a therapeutic candidate for androgenetic alopecia.

This study found that Ang1 improved survival and proliferation in human follicle dermal papilla cells under DHT-induced stress, suggesting potential as a therapeutic candidate for androgenetic alopecia.

This study reports that the loss of Langerhans cells in lichen planopilaris scars may be linked to the downregulation of ITG αvβ6, which is not seen in other scar formation diseases.

In human hair follicle keratinocytes, this study found that treatment with the pharmacological inhibitor QLT0267 led to a strong inhibition of proliferation and migration and induced nearly 100% apoptosis.

This study found that integrin alpha-6 and p63 may play a role in hair loss, with variable expression patterns in different types of alopecia observed in scalp biopsy samples.

This study found that αvβ6 integrin inhibits keratinocyte proliferation during wound healing and hair regeneration, suggesting its downregulation may enhance recovery and influence epidermal stem cell behavior.

This study found that β1 integrin-mediated signaling is crucial for the survival, adhesion, and migration of epithelial progenitor cells in human scalp hair follicles, with varying responses observed among cell subpopulations.

This study suggests that the anchorage of the arrector pili muscle to the extracellular matrix is likely mediated by α5β1 integrin, with α1β1 integrin involved in muscle cell-cell adhesion.

This study found that β1 integrin expression may serve as an indicator of androgenetic alopecia severity and could be involved in the disease's development.