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This study found that skin fibroblasts in mice arise from two distinct lineages which contribute differently to dermal structure and repair, impacting hair follicle formation during wound healing.

This review discusses the origins, differentiation, and function of dermal fibroblasts in skin development and healing, reporting no new clinical results.

This study found that CXCL12+ fibroblast subsets in mouse skin play a critical role in recruiting neutrophils and defending against S. aureus infection, with similar fibroblast activity observed in human psoriatic skin.

This review discusses the heterogeneity of dermal fibroblasts in healthy mouse and human skin and reports no clinical results; the authors highlight potential insights into physiological and pathological wound healing.

This study identified two distinct fibroblast subsets in mouse skin, revealing that adult skin scarring occurs due to the repair process utilizing only one, lineage-restricted fibroblast type instead of coordinated diverse populations.

This study found that while 450nm blue light can inhibit collagen and induce oxidative stress in dermal fibroblasts, 850nm near-infrared light may enhance metabolic activity without causing oxidative damage, suggesting potential for tailored light therapies in skin treatments.

The authors concluded that the dermal response to epidermal Wnt/β-catenin signaling depends on distinct fibroblast lineages, with each responding to different paracrine signals such as Hedgehog and TGF-β.

This study identified two cell surface markers, FAP and CD90, that distinguish between papillary and reticular fibroblasts in human skin, suggesting distinct functions and distribution in dermal layers.

This study found that Ng2+ perivascular cells in mouse skin are a diverse lineage-restricted population primarily recruited from papillary or reticular fibroblast lineages during wound healing, maintaining heterogeneity in both wounded and non-wounded skin.

This study suggests that human skin contains distinct fibroblast subsets with unique expression profiles and functions, which can be isolated to investigate their role in skin pathogenesis.

This review explores fibroblast heterogeneity in the mammalian dermis and suggests potential therapeutic applications by targeting fibroblast subtypes, but reports no new experimental results.

This study found that Dermal Fibroblast Progenitors have repressed chromatin profiles which hinder their ability to reform skin in allograft assays despite their differentiation potential.

The study found that dermal EZH2 plays a crucial role in coordinating dermal fibroblast differentiation and epidermal development by modulating Wnt/β-catenin and retinoic acid signaling.

This study investigated dermal fibroblasts in mouse skin using single-cell RNA sequencing and identified signaling pathways that influence adipogenesis, finding that IL-1-NF-κB promotes, while WNT-β-catenin inhibits, the adipogenic potential of these cells, with implications for wound healing and scar formation.

This review explores the evolution and development of skin-associated adipose tissue and proposes new nomenclature for the cells and adipose tissue underlying the reticular dermis, without reporting clinical results.

This study found that the loss of papillary fibroblasts in the skin due to UV radiation is mainly caused by an uncontrolled inflammatory response, with T cells helping fibroblast survival.

This study found that chronic UVR exposure in mice and humans leads to a permanent loss of papillary fibroblasts in the upper dermis, which is associated with changes in the extracellular matrix.

This review outlines the various fibroblast subsets in the skin dermis, their origins, and their influence on epidermal stem cell behavior, highlighting the role of the local dermal niche in stem cell plasticity.

This study observed that aging leads to significant structural and biological changes in the scalp's hair follicle environment in women, which may affect hair growth.

This study suggests that typical skin lesions in Carney complex may originate from the pro-melanogenic activity of a specific dermal fibroblast population influenced by PKA signaling.

This study found that UV radiation-induced fibroblast depletion in the skin is primarily due to a deregulated inflammatory response, with T cells aiding fibroblast survival under stress.

This study found that upper wound fibroblasts are crucial for hair follicle regeneration during wound healing and suggests that these cells, along with papillary fibroblasts, migrate within the wound.

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 discusses the role of fibroblast heterogeneity in determining skin scarring versus regeneration and reports no new results, highlighting opportunities for developing antiscarring therapies.

This study found that in murine dermis, fibroblast state switching between proliferation and ECM deposition plays a crucial role in tissue architecture and wound healing.

In this study, researchers found that skin pigmentation alterations in a mouse model of Carney complex may be caused by specific dermal fibroblasts promoting melanogenic signaling.

This review discusses the developmental origins and diversity of dermal fibroblasts, focusing on their roles in epidermal and hair follicle growth, but reports no clinical results.

In this source, recent single-cell RNA-sequencing advances reveal significant transcriptional heterogeneity among skin fibroblasts, and the discussion focuses on the distinct subtypes' roles in skin homeostasis, repair, and their evolution in fibrotic diseases like keloid scars and cancer.

This study revealed gene expression patterns in yak hair follicles during different growth phases, enhancing the understanding of cell fate specialization and providing insights for yak villus development.

In this study, deleting the transcriptional pause factor Nelfb in mouse preadipocyte lineages led to defective dermal fat formation and lethal outcomes, while interventions targeting Pparg could rescue adipocyte differentiation and promote dermal white adipose tissue formation, underscoring Nelfb's critical role in adipogenesis.