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signaling protein that, when suppressed, may grow hair by reducing inflammation and stem cell loss
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5 / 15 resultslearn Follistatin
glycoprotein that inhibits TGF-β and promotes hair growth by antagonizing activin
learn PP405
mitochondrial pyruvate carrier (MPC) inhibitor by Pelage in early trials
learn Microneedling
technique to create small wounds in skin to activate collagen production and hair growth
learn Scalp Micropigmentation
scalp tattoos to mimic the appearance of light stubble
Research
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research Structural and Biochemical Changes Underlying a Keratoderma-Like Phenotype in Mice Lacking Suprabasal AP1 Transcription Factor Function
Inhibiting AP1 in mice skin causes structural changes and weakens the skin barrier.
research The Role of ATP-Dependent Chromatin Remodeling in the Control of Epidermal Differentiation and Skin Stem Cell Activity
ATP-dependent chromatin remodeling is crucial for skin development and stem cell function.
research All Roads Lead to the Nucleus: Integration of Signaling, Transcription Factor-Mediated, and Epigenetic Regulatory Mechanisms in the Control of Skin Development and Regeneration
The nucleus is key in controlling skin growth and repair by coordinating signals, gene regulators, and epigenetic changes.
research GRHL3 Binding and Enhancers Rearrange as Epidermal Keratinocytes Transition Between Functional States
GRHL3 is important for controlling gene activity in skin cells during different stages of their development.
research DNA Methylation as an Epigenetic Memory Keeper During Skin Development and Regeneration
DNA methylation is essential for skin and hair follicle development, and could be a target for treating skin diseases.
Community Join
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community Minoxidil Response Bottlenecks: Why Sulfation and Transport Matter (And Where Tretinoin Fits In)
Minoxidil's effectiveness is limited by the need for sulfation and proper transport to hair follicles, with tretinoin potentially enhancing its effects by promoting enzyme activity and keratinocyte differentiation. Tretinoin may improve minoxidil's response by boosting the expression of necessary enzymes and transporters.
community A concise, easy-to-understand post on Androgenic Alopecia theory and its practical applications
The mechanism of Androgenic Alopecia and practical applications of treatments like Minoxidil, Finasteride, RU58841, dermarolling, scalp massages, anti-fungals, progesterone, estrogen, PPAR-γ activators, reducing oxidative stress, and scalp exercises. It explains why DHT is important in AA and how other factors might be involved such as hypoxia, increased DKK-1 expression, morphological changes to the scalp, skull growth during childhood/puberty, and blood flow.
community The Real Cause Of Androgenetic Alopecia
Androgenetic alopecia is caused by DHT affecting hair growth. Finasteride and minoxidil are used to manage hair loss by blocking DHT and promoting hair growth.
community Verteporfin and Microneedling
Clinical studies by Dr. Barghouthi and Dr. Bloxham indicate that Verteporfin, when used with FUE and FUT hair transplantation methods, shows promise in hair follicle regeneration and minimal scarring due to its ability to inhibit Yes-associated protein (YAP). Microneedling at depths of 3-3.5mm, combined with Verteporfin, could potentially reactivate dormant follicles, although the optimal dosage and application method are still under investigation. Concerns remain about the DHT sensitivity of regenerated follicles, highlighting the need for further research to optimize trauma levels and Verteporfin concentrations to achieve effective and scar-free hair regeneration.
community Compressed part of research of theory of androgenic/anabolitic balance. AGA h-responders analytic. Theory of physio-metabolitic method of anti AGA treatment
The treatment for androgenetic alopecia involves using finasteride and minoxidil with intense exercise and cold exposure to boost metabolism and reduce androgenic effects, potentially leading to hair regrowth. This approach may activate biological pathways for improved hair and overall health.