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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 review discusses the development, lineages, functions, and roles of fibroblasts in fibrosis across four organs, highlighting their capabilities in tissue repair and contributions to fibrotic disorders when aberrantly activated, but it reports no new experimental findings.

This research observed that EGFR activity appears to maintain hair follicle quiescence and immune privilege, and its inhibition may lead to stem cell apoptosis and scarring alopecia during inflammation.

This study reported that in mouse models, deletion of EGFR resulted in stem cell hyper-proliferation followed by apoptosis, leading to scarring alopecia, and implicated EGFR's role in maintaining hair follicle quiescence and immune privilege during inflammation.

This study found that α-MSH acts as a modulator of inflammatory and fibrogenic responses in human fibroblastic skin cells, indicating potential therapeutic options for fibrotic skin disorders and inflammatory diseases of the hair follicle.

Discoid lupus erythematosus involves immune activation and fibrosis around hair follicles, with shared pathways across humans, dogs, and mice, suggesting potential treatments for both humans and animals.

This research observed that diabetes impairs wound healing in mice by disrupting key mechanotransduction pathways in fibroblasts, which are crucial for the healing process. The study also suggests transcriptomic changes could inform future diabetic wound repair therapies.

In this study, researchers found that extrafollicular progenitors marked by Hic1 are the main contributors to reparative fibroblasts in wound repair, with potential to modulate healing outcomes through genetic and pharmacological interventions.

This review discusses the mechanisms of wound healing and excessive scarring, highlighting the importance of understanding these processes for developing new therapies to prevent fibrotic scarring in large skin wounds.

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 reports that in systemic sclerosis, CD34+ dermal fibroblasts transition to CD34−, podoplanin+, and CD90+ fibroblasts across the dermis, suggesting a role in unchecked fibrosis.

This study observed that post-surgical use of chlorhexidine digluconate mouth rinse in patients may induce a fibrotic transformation in gingival tissue, promoting a scar-like wound healing response.

Fibroblasts are crucial in scar formation and wound healing, with potential therapies aiming for scarless healing.

This review explores the molecular mechanisms through which NGF may enhance burn wound healing by reducing healing time and improving scar quality, but it presents no new clinical results.

This study examined the effects of WNT10B on dermal papilla cells in vitro, finding that it alters gene expression, decreases protein synthesis, and upregulates a specific signaling pathway, potentially influencing hair follicle morphogenesis.

CCCA may be a fibroproliferative disorder, and anti-fibrotic therapies could help.

This review article addresses how the TRPV4 ion channel helps cells respond to mechanical and environmental stimuli, discussing its role in calcium signaling crucial for tissue repair and fibrosis across various organ systems, and highlighting potential therapeutic targets from animal and disease models.

In this study, researchers used a mouse model to demonstrate that expression of MARCKSL1 in dendritic cells plays a crucial role in modulating fibrotic responses and scar formation during wound healing, suggesting that targeting this expression could offer new therapeutic strategies for scar prevention.

This study found that blocking the chemokine CXCL12 in a testosterone-induced mouse model of androgenetic alopecia restored hair regeneration and reduced fibrosis and immune alterations.

In this study, researchers found that both Wnt/β-catenin and Hedgehog signaling pathways must be activated in wound fibroblasts to promote hair follicle neogenesis in mice, suggesting these pathways are crucial for regenerative healing strategies.

This review focuses on the role of the transcription factor Foxn1 in skin biology and discusses its potential implications for regenerative medicine, but reports no new clinical results.

This study found that certain T cell-associated genes were upregulated in dogs with Vogt-Koyanagi-Harada syndrome and vitiligo, suggesting a shared immunopathogenesis with humans.

This study highlighted the effectiveness of HT-scCAT-seq as a tool for understanding gene regulation in single cells, offering insights into embryonic skin development and proposing a framework for exploring regulatory mechanisms in various biological and disease contexts.

This study found that PBMCsec has anti-fibrotic effects on mouse and human skin scars by regulating pro-fibrotic gene expression and inhibiting myofibroblast differentiation and elastic fiber breakdown.

The researchers reported that targeting glycoprotein 130's signaling site in animal models promoted tissue regeneration and reduced osteoarthritis progression through anti-inflammatory and protective effects.

Alopecia totalis/universalis involves more intense immune activity and inflammation than patchy alopecia areata.

This review examines the mechanisms behind pathological scarring like hypertrophic scars and keloids, highlights the limitations of current treatments, and suggests that biomaterial-enabled delivery of anti-fibrotic statins, such as atorvastatin, may offer a promising therapeutic avenue for managing these scars.

This review explores current knowledge on fibroblast lineage specification and its impact on scar-free wound healing, noting that early fetal skin fibroblasts support regeneration, while later developmental shifts lead to fibrosis, highlighting potential strategies to reprogram adult fibroblasts for regenerative repair.

This review suggests that metformin, known for its antidiabetic uses, may benefit chronic inflammatory skin diseases like acne vulgaris, hidradenitis suppurativa, and rosacea due to its multiple therapeutic properties, although more research is needed to confirm its efficacy in dermatology.

In this study, researchers found that disrupting EGFR signaling in mice led to increased inflammation and hair follicle damage but that inhibiting the JAK-STAT1 pathway could restore hair growth and skin function.