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This study found that Smad7 perturbs hair follicle development while promoting sebaceous gland formation by antagonizing Wnt/β-catenin signaling in transgenic mice.

In this study, human bone marrow mesenchymal stem cell-derived exosomes significantly accelerated cutaneous wound healing in rats by modulating the TGF-β/Smad signaling pathway.

This study found that overexpression of Smad7 in transgenic mice led to severe alterations in multiple epithelial tissues, resulting in early death after birth.

This study found that BMP-2 activates Dlx3 gene transcription in murine keratinocytes by binding with Smad1/Smad4, suggesting a mechanism for BMP signaling's role in skin and hair follicle regulation.

This study concluded that the 800-nm diode laser is effective in enhancing skin structure and collagen expression via the TGF-β/Smad pathway, suggesting potential for non-ablative rejuvenation.

This review examines the roles of Smad-4 and Smad-7 in hair follicle differentiation and development through BMP signaling and TGFβ/Activin/BMP pathway inhibition but reports no new experimental results.

This study found that disrupting Smad4 signaling in young mice led to overactivation of follicle stem cells, causing hyperplasia and depletion of the stem cell niche.

This study found that the loss of Smad4 in keratinocytes reduces Dsg4 expression via disrupted BMP signaling, contributing to hair follicle degeneration and alopecia.

This study found that keratinocytes show increased expression of the TGF-β system and collagen type I with age, suggesting a heightened profibrotic response during skin differentiation associated with scarring.

This study found that in vivo bioluminescence can track Smad2/3-dependent TGF-β signaling during the wound healing process in mice, with signaling increasing after healing rather than immediately post-wounding.

This study observed that reduced activation of SMAD2/3 proteins in cutaneous squamous cell carcinoma tissue compared to adjacent tissue may indicate a tumor suppressor role in disease progression.

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.

This study found that miR-370-3p targets SMAD4 to inhibit cell proliferation, promote apoptosis, and affect the cell cycle in follicular papilla cells, demonstrating differences in their expression in sheep tissues, which may impact hair follicle development.

This study found that hair follicle mesenchymal stem cells improved liver function and pathology in a mouse model of liver cirrhosis, potentially by inhibiting the TGF-β/Smad pathway and reducing hepatic stellate cell activation.

This study observed that a CARASIL mouse model demonstrated abnormal behavior, vascular and cellular changes, and upregulation of the TGF-β/Smad signaling pathway, indicating its potential involvement in CARASIL pathogenesis.

This study found that SMAD2 overexpression in human hair follicle stem cells promoted differentiation and apoptosis while inhibiting proliferation, and Smurf2 upregulation limited mouse wound healing by suppressing the SMAD2/NANOG/DNMT1 axis.

This study found that human bone marrow mesenchymal stem cell-derived exosomes promote cutaneous wound healing in rats by inhibiting the TGF-β/Smad signaling pathway.

This study found that deleting Smad2 and Smad3 in murine skin leads to severe skin abnormalities and cancerous lesions, similar to but more severe than those seen in Smad4 mutants, indicating the critical role of TGF-β signaling in skin development.

This study found that all-trans retinoic acid (ATRA) inhibits proliferation and promotes apoptosis in secondary hair follicle-derived dermal papilla cells from cashmere goats, likely via the TGF-β2/Smad2/3 signaling 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 research found that kaempferol, a flavonoid from hair growth-promoting plants, significantly enhanced human dermal papilla cell proliferation and inhibited specific signaling pathways, outperforming minoxidil, with topical application in mice promoting hair growth and thickness, indicating potential as a natural hair loss treatment.

This study found significantly higher P-Smad2 levels in both lesional and nonlesional skin of organ transplant recipients, suggesting elevated TGF-β signaling might contribute to their increased cancer susceptibility.

In this study with mice, simultaneous inactivation of Smad4 and PTEN genes led to rapid development of invasive forestomach squamous cell carcinomas, mirroring human esophageal SCCs.

In this study, the deletion of Smad4 and PTEN genes in mice was associated with rapid and invasive squamous cell carcinoma formation in the forestomach, modeling human esophageal cancer progression.

This study found that exosomes derived from human bone marrow mesenchymal stem cells significantly promote cutaneous wound healing in rats by modulating the TGF-β/Smad signaling pathway.

This study found that exosomes from adipose mesenchymal stromal cells, particularly those carrying miR-122-5p, may enhance hair follicle regeneration in androgenic alopecia by targeting the TGF-β/SMAD3 axis.

This study suggests that canonical BMP signaling, particularly involving Smad1 and Smad5, plays a critical role in hair follicle stem cell regulation and hair morphogenesis, with distinct roles from pSmad8.

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

This study suggests that the down-regulation of 14-3-3 proteins in wild-type keratinocytes, absent in Smad4 mutant keratinocytes, might contribute to the failure of hair follicles to initiate catagen in Smad4 knockout mice.

This study found that miR-203a-3p downregulates Smad1, promoting the differentiation of loureirin A-induced hair follicle stem cells, suggesting it could be a potential therapeutic target for skin wound healing.