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This study suggests that targeting the increased expression of SIX1 in systemic sclerosis may be a viable strategy for addressing dermal fibrosis.

This study identified a new role for IL-4Ra-induced oxidative metabolism in wound macrophages, essential for balancing inflammatory response and promoting pro-fibrotic repair, suggesting a target for fibrosis prevention.

This study found that ACKR2 plays a crucial role in reducing inflammatory skin fibrosis and promoting inflammation resolution through IFN‐β production, limiting tissue scarring.

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 used advanced RNA sequencing techniques to discover that communication between specific fibroblast and myeloid cell populations may play a role in acne keloidalis, and found that corticosteroid injections could significantly reduce disease activity and gene expression related to these cells.

In this study, researchers found that the compound BMS-470539 induced a senescence-like state in fibroblasts from systemic sclerosis patients, reducing fibrosis-associated markers in vitro and decreasing skin thickness in a mouse model of skin fibrosis, suggesting a novel therapeutic strategy for managing fibroblast-driven diseases.

In this study, researchers developed an axolotl skin-derived extracellular matrix scaffold that enhanced wound healing in mice by promoting skin regeneration and reducing fibrosis, offering potential as a regenerative biomaterial for clinical use.

This study demonstrated that SHFKO significantly accelerated healing in acute radiation-induced skin injuries, with mechanisms involving apoptosis inhibition, suppression of inflammation, and restoration of ROS balance, suggesting its potential as a novel multi-target therapy for radiodermatitis.

This study found that Wnt1/βcatenin signaling plays a crucial role in activating the epicardium and cardiac fibroblasts, which supports cardiac repair following acute ischemic injury.

This study found that TGFbeta is a key pathway causing age-related loss of dermal fat's antimicrobial function, suggesting that targeting TGFBR might help restore skin defense against infections in older age.

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 study found that fibroin/gelatin and spidroin microparticles increased re-epithelialization rates and inhibited scar formation in mouse models of deep skin wounds.

This review discusses the role of the long form of thymic stromal lymphopoietin in cutaneous immune-mediated diseases and reports no new results.

This review highlights the potential of amphiregulin as a therapeutic target, noting its role in both fibrotic and malignant diseases, and discusses promising early findings but reports no new clinical results.

This review discusses Amphiregulin (AREG) as a potential target for treating fibrotic disorders and cancer, highlighting its role in disease progression and promising results in preclinical studies and early trials.

This study found that Annexin A5 significantly reduced fibrosis and inflammation in both preventive and therapeutic contexts in a bleomycin-induced localized scleroderma mouse model, demonstrating its potential anti-fibrotic and anti-inflammatory effects for treating fibrotic diseases.

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.

This article discusses the advances in understanding wound-induced hair follicle neogenesis (WIHN) and highlights the roles of specific signaling pathways and cellular plasticity, noting no clinical results but suggesting potential areas for further research.

This review discusses the evolution of adipose tissue research in regenerative medicine, from tissue transfer to cell-free bioengineering applications, highlighting its therapeutic potential, current limitations, and future directions.

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 synthesizes knowledge of how dendritic cell signals, epithelial integrins, and fibroblast activity converge on TGF-β1 to maintain or disrupt skin healing, contrasting normal and fibrotic scar formation and suggesting possible integrin and immune-targeted treatments for skin fibrosis.

In laboratory research, investigators found that apoptotic vesicles from interleukin-10-treated fibroblasts promote wound healing and reduce fibrotic scarring by enhancing mitochondrial function, modulating collagen composition, and inhibiting the Hedgehog signalling pathway, offering potential for regenerative medicine applications.

This comprehensive review suggests that CD44 signaling plays a significant role in post-natal skin wound healing and scar formation, with potential for therapeutic approaches targeting CD44 to shift from fibrotic scarring towards regenerative healing, including wound regeneration and hair neogenesis.

This study found that the antiviral drug daclatasvir significantly improved fibrosis and quality of life in a mouse model of recessive dystrophic epidermolysis bullosa, suggesting potential for treating this and other fibrotic diseases.

This review explores recent advances in inflammation resolution and considers how macrophage reprogramming might help address severe COVID-19 outcomes, particularly those involving cytokine storms, but it reports no new experimental results.

This study introduces a novel in vitro model for clubfoot fibrosis to enable high-throughput drug screening and found that while the model increased collagen deposition, the antifibrotic drug minoxidil effectively inhibited the expression of collagen cross-linking enzymes.

In this animal study, ginsenoside Rb1 demonstrated therapeutic effects on hypertrophic scar remodeling, with the highest efficacy observed at a dose of 0.56 mg.

This study found that sustained ERK activity during tissue regeneration in spiny mice is linked to fibroblast growth factor and ErbB signaling, while inhibiting ERK shifted regeneration toward scarring.

The study suggests that integrin β1 is crucial for maintaining liver microstructure and its absence may promote fibrosis by disrupting hepatocyte-extracellular matrix interactions and increasing TGF-β secretion.

AKR1B10 enzyme may cause keloid scars and could be a treatment target.