Search

everythingexperts & clinicslearnfaqsresearchcommunity

for

Search:↓

This study identified that in mice, sweat gland development is directed by mesenchymal signals that suppress SHH-production, while in humans, this occurs through a BMP spike in embryonic development.

In this study, fingertip regeneration in mice was associated with specific signaling pathways involving hair follicles and hedgehog signaling, with potential implications for improving human hand injury treatments.

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 the acceleration of endothelial to mesenchymal transition due to loss of Notch signaling led to delayed wound healing and increased scarring in skin wounds.

This study introduces a method using lentiviral delivery in mice to expedite analysis of factors crucial for hair follicle morphogenesis by enabling rapid gain- or loss-of-function studies.

This study found that stabilizing β-catenin in a specific mouse model led to temporarily increased hair density but ultimately accelerated hair follicle aging and hair thinning.

This study found that a hypoxic microenvironment enhanced the proliferation and pluripotency of adipose mesenchymal stem cells, promoting hair follicle formation and upregulating specific growth factors in Arbas Cashmere goats.

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.

This study describes a method using lentivirus in mouse cells to analyze epithelial-mesenchymal signaling important for hair follicle development, offering a quicker alternative to genetic models.

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 review discusses the advancements in intraoperative stem cell therapies and highlights their potential to improve hair regrowth, but it reports no new clinical results.

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

This study found that human umbilical cord mesenchymal stem cells (hUCMSCs) promoted hair regeneration in androgenetic alopecia model mice by activating Wnt/β-catenin signaling, enhancing hair follicle stem cell proliferation, and reducing dermal papilla cell apoptosis.

This study found that epidermal growth factor significantly enhances the proliferation of hair follicle-derived mesenchymal stem cells through the EGFR/ERK and AKT pathways, without involving the STAT3 pathway.

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 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 umbilical cord mesenchymal stem cell-derived exosomes improved hair growth in mice with androgenetic alopecia by promoting hair follicle stem cell stemness through the RAS/ERK pathway, suggesting a potential new treatment strategy for this condition.

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 pretreatment with a PPAR-γ modulator may prevent damage to hair follicle stem cells caused by a chemotherapy metabolite, potentially offering a strategy to mitigate permanent chemotherapy-induced alopecia.

This study discovered that exosomes from adipose-derived mesenchymal stem cells can mitigate damage in dermal papilla cells by modulating the TGF-β1/SMAD2 signaling pathway through miRNAs miR-574-3p and miR-125a-5p, revealing potential therapeutic targets for androgenetic alopecia.

This study found that hypoxia-preconditioned HF-MSC-derived exosomes improved therapeutic outcomes in models of ulcerative colitis, potentially through miR-214-3p-mediated pathways affecting mitochondrial function and inflammatory responses.

In this study, exosomes from hypoxia-conditioned mesenchymal stem cells significantly improved SOCS3 and STAT3 expression in a mouse model of androgenetic alopecia, suggesting they may offer a more effective therapeutic approach than minoxidil by restoring follicular homeostasis.

This study found that PBX1 enhances the proliferation and reprogramming of hair follicle mesenchymal stem cells by activating the AKT/GSK3β signaling pathway, promoting NANOG expression, and inhibiting apoptosis.

This study found that coadministration of pimecrolimus may interfere with the therapeutic efficacy of mesenchymal stem cell therapy in atopic dermatitis.

This study found that selective androgen receptor modulators (SARMs) significantly inhibited tumor growth and metastasis-promoting factors in AR-positive triple-negative breast cancer models.

This study reported that high-intensity red LED irradiation increased osteogenic differentiation and mineralization of human bone marrow mesenchymal stem cells, potentially through Wnt/β-catenin pathway activation.

This study reports that the maintenance and morphogenesis of skin appendages rely on both the dose and duration of ectodysplasin signaling.

This study found that the protein MIM is crucial for maintaining cilia and Sonic hedgehog signaling in mesenchymal cells by counteracting Src-mediated phosphorylation of Cortactin, impacting hair follicle formation.

This study identified a distinct CD49fhigh mesenchymal stem cell subpopulation in the dermis that supports hair follicle development and maintenance via Notch signaling activation.

Tissue stiffness affects sweat gland development by guiding cell differentiation through specific signals.