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PRO-C22 can help diagnose and monitor the severity of hidradenitis suppurativa.

This study found that hidradenitis suppurativa is associated with increased serum levels of hypoxia-inducible factor-1α, suggesting its role in the disease's pathogenesis and as a treatment target.

This study created transgenic mouse models with the LMNA gene mutation common in Hutchinson-Gilford progeria syndrome, revealing skin and teeth abnormalities related to transgene expression levels.

This study found that skin organoids derived from iPSCs with an HS-associated NCSTN mutation showed defects in hair follicle stem cell differentiation and increased expression of inflammatory proteins related to hidradenitis suppurativa.

This study suggests that the HCR risk allele within the PSORS1 locus may contribute to psoriasis susceptibility by altering gene expression related to skin structure and differentiation, although these changes alone might not result in clinical symptoms.

In this study, researchers found that correcting the HGPS mutation with Adenine base editing partially rescued accelerated skin cell differentiation and reduced cell death in patient-derived stem cells.

This article reviews treatments for progeria, including aspirin, hydrotherapy, and farnesyl transferase inhibitors, but reports no new clinical results.

This review discusses genetic mutations associated with Hutchinson-Gilford progeria syndrome and reports no clinical results; the authors emphasize the importance of cardiovascular monitoring in management.

This study found that hair follicle stem cells from hidradenitis suppurativa patients showed alterations in cell cycle regulation and DNA replication, potentially linking genetic predisposition to the skin inflammation characteristic of the disease.

This study reports that some human cell surface HLA-I molecules (including HLA-B27) can appear without their usual peptide component, potentially altering immune interactions, influencing arthritis development in specific mice models, and exhibiting upregulation in certain cancer cells.

This study demonstrates that human epidermal stem cells can adapt to environmental temperature changes through mTOR signaling, and prolonged inhibition of mTORC1 supports stem cell maintenance, which may be vital for regenerative medicine.

This research reexamined transcriptomic data to study stem and progenitor cell proliferation in psoriasis, finding that the number of committed progenitor cells increased eight-fold in psoriatic skin without altering stem cell numbers, potentially identifying new therapeutic targets.

This study suggests that Keratin 6hf may be a potential marker of oral squamous cell carcinoma and could play a role in its progression, though further research is needed to understand its function.

This study found elevated levels of IL-18 and free IL-18 in hidradenitis suppurativa patients compared to healthy controls, suggesting these cytokines may serve as novel biomarkers for disease activity, with correlations indicating their involvement in disease severity.

This article offers a viewpoint on hidradenitis suppurativa pathogenesis, suggesting that impaired Notch signalling from γ-secretase mutations may drive inflammation and link the condition to other Th17-driven diseases.

This study found that Rab5c is crucial for proper HSPC development in zebrafish embryos by regulating Notch and AKT signaling through endocytic trafficking, with both deficiency and overactivation leading to production defects.

This study found that RSPO1 mutations in patients with a 46XX disorder of sexual development contribute to impaired skin integrity and increased risk of squamous cell carcinoma in areas subject to friction.

This study observed that male patients with alopecia areata had elevated serum levels of HSP70 and IL-15, with levels increasing alongside disease severity, suggesting these markers are strongly associated with the disease's pathogenesis.

This study found that the mutant hairless rhino bald protein in mice interacts with the vitamin D receptor but cannot repress its transactivation and shows abnormal cellular localization.

This study found that DC-HIL+ myeloid derived suppressor cells are increased in the blood and skin of patients with cutaneous lupus erythematosus and show immunosuppressive properties.

This study found that the transcription factor p63 is crucial for horizontal basal cell differentiation in the olfactory epithelium, suggesting a p63-dependent mechanism activates reserve stem cells after injury.

This study found that a hypomorphic mutation in the Hr gene contributes to the development of diet-induced pruritic atopic skin in mice, particularly when combined with dietary deficiencies of polyunsaturated fatty acids and starch.

This study found that in Hutchinson–Gilford progeria syndrome, iPSCs committed to the keratinocyte lineage faster than normal cells, with LEF1 expression reduced and a partial rescue of the phenotype achieved through adenine base editing.

This study found that skin mesenchymal stem cells from hidradenitis suppurativa patients overexpress proinflammatory and anti-inflammatory cytokines, suggesting their potential contribution to the disease's pathogenesis.

In a human genetic study on hidradenitis suppurativa, researchers identified 12 genetic risk loci and found that CXCR4-CD74 signaling may play a key role in hair follicle inflammation, suggesting CXCR4 blockade as a potential therapeutic approach for this condition.

This study found that in hidradenitis suppurativa, the proteins SERPINB3/B4 and S100A7/A8/A9 were significantly overexpressed in lesional skin compared to nonlesional skin, suggesting new pathways in the disease's pathogenesis.

This study provides evidence that ILC1-like cells can induce alopecia areata in previously healthy human hair follicles, challenging the view that it is solely an autoantigen-dependent autoimmune disease.

This study found that HPV8-induced actinic keratoses may mechanistically involve Lrig1+ hair follicle keratinocyte stem cells, with the E6 gene promoting downstream STAT3 activity in a mouse model.

This study found that the HS III element in the K14 gene's regulatory sequence promotes gene expression in inner root sheath keratinocytes, highlighting cooperative interactions in keratinocyte-specific gene regulation.