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In a depilated mouse model, this study found that blocking CXCL4 activity with an anti-CXCL4 monoclonal antibody promoted hair growth by inducing an earlier anagen phase, delaying hair follicle regression, and altering expression of genes and proteins related to hair growth and cell proliferation.

This study demonstrates that SDF-1/CXCL12 and CXCR4 signaling play a crucial role in directing the migration and positioning of melanoblasts in mouse hair follicle formation.

This study found that far-infrared radiation preconditioning significantly enhanced the proliferation, survival, and migration of bone marrow-derived stem cells in vitro, indicating potential therapeutic benefits for cardiac ischemia treatment.

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 study found that higher serum CXCL10 levels may predict the progression of non-segmental vitiligo, especially in patients also suffering from autoimmune thyroid disease and/or alopecia areata.

This study found that specific SNPs in the CXCL1 and CXCL2 genes may be associated with increased susceptibility to alopecia areata in the Korean population.

In this study, researchers prepared a humanized CXCL12 antibody for alopecia areata treatment, finding it significantly delayed disease onset in mice and reduced immune cell activation, suggesting potential as an immune modulatory therapy.

This study found that combining LED yellow light with an engineered strain expressing CXCL12 improved wound healing and reduced inflammation in a mouse model of scald wounds.

In this study, increased production of CXCL10 was associated with the infiltration of Th1 and Tc1 cells in acute alopecia areata, suggesting a possible new target for treatment.

This study found that Plerixafor, a CXCR4 antagonist, promotes melanogenesis in melanocytes by increasing MITF and tyrosinase expression and enhancing melanocyte migration, and it effectively restores pigmentation in a mouse depigmentation model without toxicity, highlighting its potential for treating pigmentary disorders.

This study concluded that the CXCL12–CXCR4 signaling pathway significantly contributes to hair loss in androgenetic alopecia and alopecia areata by promoting inflammation and fibrosis, whereas inhibiting this pathway can restore hair growth and follicle health.

In this study, plerixafor was found to enhance melanogenesis and promote repigmentation by engaging a β-arrestin–β-catenin–MITF signaling axis in melanocytes, and showed effectiveness in restoring depigmentation in a murine model without causing systemic toxicity.

This study found that exosomes derived from hypoxia-conditioned mesenchymal stem cells modulated inflammatory biomarkers by decreasing CXCL12 and increasing IL-10 expression in a DHT-induced androgenic alopecia mouse model, indicating potential for treating hair loss through immunoregulation.

This study found that regulatory T cells accumulate in hair follicle epithelium via the Cxcr4-Cxcl12 axis, partially influenced by glucocorticoid receptor signaling, promoting hair regeneration; similar mechanisms were observed in human and murine skin.

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.

This study reported that CXCL12 may have a dual role in alopecia areata, where decreased levels could impair angiogenesis and disrupt vascular support to hair follicles, while its overexpression might exacerbate autoimmune attacks on hair follicles, contributing to hair loss.

This study observed that CXCL12 is highly co-expressed with androgen receptors in human hair follicle cells, and its inhibition via antibodies increased hair length, suggesting a potential treatment strategy for androgenic alopecia.

This study found that subcutaneous injection of a CXCL12 neutralizing antibody significantly promoted hair growth in androgenic alopecia and inhibited hair loss in alopecia areata in mouse models, suggesting its potential as a promising treatment for hair loss.

This study found that CXCL12 inhibits hair growth via the CXCR4/STAT signaling pathway, suggesting that targeting this pathway could be a promising approach for promoting hair growth.

This study found that disrupting Sdf1-Cxcr4 signaling promoted tissue regeneration in wild-type mice, hinting at potential strategies to induce such regeneration in mammals.

In this study, researchers reported that specific gene polymorphisms in Jiangnan cashmere goats, particularly SNPs in the HOXC13 and WNT4 genes, were significantly associated with key economic traits like birth weight and yearling weight, providing molecular markers for breeding and enhancing economic trait stability.

This study suggests that the CXCL8 gene may regulate cashmere fineness in Liaoning cashmere goats, providing new insights into the cellular mechanisms of cashmere growth and quality.

This observational study concluded that anti-Ku antibodies do not specifically indicate any systemic autoimmune disease or associated clinical phenotype.

This case study reported significant but temporary hair regrowth and skin repigmentation in a patient with vitiligo and alopecia areata during treatment with oral ruxolitinib.

This study investigated the impact of the JAK inhibitor ruxolitinib on APS-1 patients, reporting that treatment decreased excessive T-cell-derived interferon-γ, normalized inflammatory markers, and led to remission of several autoimmune symptoms without serious adverse effects.

In this study, oral tofacitinib treatment led to significant hair regrowth and changes in skin and blood biomarkers in a patient with alopecia areata.

In this study, blocking the CXCR3 receptor in mice prevented the development of alopecia areata by inhibiting the accumulation of specific T cells in the skin, suggesting a potential therapeutic approach for humans.

This study highlights the need for further research on dysregulated immune and fibrotic pathways in morphea to better understand its pathogenesis and develop new biomarkers and therapies.

This study identified chemokine receptor ligands cxcl10 and cxcl11 as new hair-specific transcriptional targets of the Eda pathway, suggesting chemokine signaling plays a role in primary hair follicle patterning.

Stretching skin increases a certain protein that attracts stem cells, helping skin regeneration.