Search

everythingexperts & clinicslearnfaqsresearchcommunity

for

Search:↓

This study found that in androgenetic alopecia patients, there is enhanced expression of type 2 TGF-β and type II receptors in hair follicles, suggesting a link to hair growth cycle changes.

This study showed that coexpression of TG2 and Gbx1 in the epidermis is necessary for esophagus-like mucosal transdifferentiation, with TGF-beta2 in the dermis essential for the process through epithelial-mesenchymal interaction.

In this study, the researchers found distinct patterns of TGF-beta 1 and IGF-II expression in pig fetal subcutaneous tissue, suggesting specific regulatory roles in developing adipocytes and muscle tissue.

This study found that trans-3,4'-Dimethyl-3-hydroxyflavanone reduces active TGF-beta2 levels in human keratinocytes, suggesting it may enhance hair growth by suppressing the TGF-beta2 activation pathway.

This study reviews evidence that in keloid development, transforming growth factor-β (TGF-β) drives fibroblast proliferation and fibrosis not only through the classical Smad-dependent pathway but also via equally important Smad-independent signaling cascades, suggesting these pathways as possible targets for more effective keloid therapies.

This study in mice suggests that defects in hair follicles with mesenchymal TSC2 disruption may result from an impaired TGFβ1 response, indicating a potential novel treatment approach for tuberous sclerosis complex.

In this study, transgenic mice with a truncated latent transforming growth factor-beta-binding protein showed reduced keratinocyte proliferation and alterations in the hair cycle due to mis-localization of transforming growth factor-beta.

ROS may affect hair loss related to hormones.

This study suggests that type IV collagenases, MMP-2 and MMP-9, play important roles in the hair cycle by regulating the expression of VEGF, IGF-1, and TGF-β in mice.

This study suggests that TGF-β receptor 1 may play a role in deer antler skin cell differentiation and dermis fibroblasts' rapid proliferation, potentially aiding the alignment of skin and cartilage growth rates in sika deer antlers.

This study found that patients with alopecia areata had higher serum TGF-β1 levels than controls, and these levels were associated with disease severity, suggesting a potential role in its pathogenesis.

This study reported that Cosmos caudatus extract alone may therapeutically modulate the AR–FGF-2 axis in a BPH rat model, comparable to finasteride, but combining them disrupted pathway regulation, increasing TGF-β levels.

In this study, individuals with androgenetic alopecia showed higher serum levels of oxidative stress markers and lower levels of antioxidants, indicating disrupted redox balance and suggesting oxidative stress may accelerate hair loss.

This study identified TGF-β2 as a crucial signal in hair follicle stem cell regeneration, highlighting its role in counteracting BMP signaling to promote tissue regeneration.

In this study, androgen did not affect keratinocyte growth in coculture with androgenetic alopecia-derived dermal papilla cells, but did significantly suppress keratinocyte growth when androgen receptor was overexpressed in the papilla cells.

This review discusses the roles of TGF-β family signaling in regulating normal and cancer stem cells and highlights the need for further research to develop potential cancer treatments; it reports no new results.

This study found that conditional expression of TGFβ1 in mice affects epidermal and hair follicle growth, with chronic expression causing severe alopecia and a negative feedback loop involving Smad7.

This study found that inhibiting TGF-β receptors in adult dermal fibroblasts restored their function and increased resistance to Staphylococcus aureus infection by enhancing their adipogenic and antimicrobial capabilities.

This study found that the transcription factor FOXO1 plays a crucial role in wound healing by protecting keratinocytes from oxidative stress and regulating TGF-β expression.

The TGF-β family helps control how cells change and move, affecting skin, hair, and organ development.

This study found that TGFβ signaling is essential for keeping sebocytes undifferentiated by reducing lipid-related gene expression, using a novel human sebocyte culture model.

This study suggests that TGF-β 2 plays a critical role in hair follicle morphogenesis and may enhance the effectiveness of future cell therapies for hair regrowth using expanded dermal papilla cells.

This study found that procyanidin B-3, a compound isolated from barley extract, may promote hair growth by enhancing hair epithelial cell growth and counteracting TGF-β1's growth-inhibiting effects in vitro and in vivo.

This review discusses the role of the CXXC5 protein as a transcription factor and signaling coordinator, noting its involvement in embryonic development, tissue homeostasis, and diseases such as tumorigenesis, but reports no new experimental findings.

This study observed that Endoglin is crucial for maintaining correct hair follicle cycling and stimulating hair follicle stem cell niches through feedback interactions involving Wnt/β-catenin and Bmp/Smad signaling pathways in a mouse model.

This study found that NFI-C plays a crucial role in the transition from the telogen to anagen phase of the hair follicle cycle, affecting hair growth initiation in mice.

TGF-β1 increases androgen receptor activity in hair loss, but Hic-5/ARA55 can counter this effect.

This study found that procyanidin oligomers from apples and barley may stimulate hair growth by promoting hair epithelial cell proliferation and protecting them from apoptosis via MEK activation in a murine model.

In this study, TGFβR I was more highly expressed in alpaca ear skin than in back skin, suggesting it may inhibit coat hair growth, with let-7b downregulating TGFβR I protein through transcriptional repression.

This study found that all-trans-retinoic acid (ATRA) inhibits mink hair follicle growth by reducing dermal papilla cell proliferation and inducing apoptosis, likely through the TGF-β2/Smad2/3 pathway.