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July 1999 in “American Journal Of Pathology” The hairless (hr) gene is essential for normal hair follicle function and its mutation leads to hair loss.
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August 2010 in “Developmental Cell” MIM is crucial for hair follicle formation and regeneration by controlling cilia formation and hedgehog signaling through its interaction with Cortactin and Src.
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February 2022 in “Seminars in cell & developmental biology” Recent findings suggest that genetic factors, immune system issues, and skin cell defects might contribute to the development of hidradenitis suppurativa.
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May 2022 in “Genes & Diseases”
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August 2019 in “American journal of human genetics” FOXN1 gene variants cause low T cells and immune issues from birth.
July 2022 in “Journal of Investigative Dermatology” Inhibiting TYK2 can restore hair growth in alopecia areata.
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March 2017 in “Scientific reports” Double-stranded RNA causes inflammation in hair follicle cells, which may help understand and treat alopecia areata.
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May 2022 in “Diagnostics” Certain genetic markers can indicate higher or lower risk for systemic lupus erythematosus.
October 2021 in “The journal of investigative dermatology/Journal of investigative dermatology” The new aptamer TAGX-0003 shows promise as an effective treatment for hair loss disorder alopecia areata.
October 2025 in “Cell Death and Disease” CD271 is crucial for maintaining healthy skin and preventing inflammation.
June 2026 in “Frontiers in Cell and Developmental Biology” LHX2 is crucial for development, tissue repair, and preventing diseases.
April 2023 in “The journal of investigative dermatology/Journal of investigative dermatology” SETDB1 is essential for controlling DNA methylation, silencing retrotransposons, and maintaining skin cell health, with its absence leading to skin inflammation and hair loss.
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July 2002 in “EMBO journal” Normal skin cell renewal doesn't need RAR signaling, but vitamin A-related skin thickening does.
April 2016 in “Journal of Investigative Dermatology” Blocking Oncostatin M's role in the JAK-STAT pathway can stimulate hair growth in mice.
April 2010 in “Cancer Research” Stat3 activation increases hair follicle progenitors but reduces bulge region stem cells.
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April 2015 in “Development Growth & Differentiation” The Hippo signaling pathway helps control organ size during regeneration by regulating gene expression.
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April 2008 in “Journal of Biological Chemistry” Hirosaki hairless rats lack hair due to missing DNA with key keratin genes.
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May 2022 in “Journal of Investigative Dermatology” Endothelial TLR2 is crucial for timely wound healing, but HFSC TLR2 is not needed.
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August 2017 in “Journal of Cellular Physiology” PD‐L1 and PD‐L2 may not effectively control immune activation in alopecia areata.
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January 2023 in “International Journal of Biological Sciences” CTHRC1 is essential for healing and preventing heart rupture after a heart attack.
Deleting the MAD2L1 gene in mice led to rapid tumor growth despite chromosomal instability.
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November 2024 in “International Journal of Molecular Sciences” YAP and TAZ proteins control skin cell growth and repair.
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July 2007 in “Development” TAF4 is important for skin cell growth and helps prevent skin cancer in mice.
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November 2017 in “Scientific Reports” The research provides a gene-based framework for hair biology, highlighting the Hippo pathway's importance and suggesting links between hair disorders, cancer pathways, and the immune system.
June 2025 in “Biomolecules” RORA affects hair follicle stem cells' structure and movement, potentially helping treat hair loss.
November 2022 in “Journal of Investigative Dermatology” Growth hormone-releasing hormone (GHRH) boosts hair growth and human scalp hair follicles have their own growth hormone system.
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June 2021 in “The Journal of Experimental Medicine” Understanding signaling in blood cells is complex and still limited.
Understanding hair follicle signaling can improve hair disorder treatments.
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August 2023 in “Autophagy” Autophagy helps control skin inflammation and cancer responses and regulates hair growth by affecting stem cell activity.