1 citations
,
December 2022 in “Frontiers in Immunology” Tissue environment greatly affects the unique epigenetic makeup of regulatory T cells, which could impact autoimmune disease treatment.
January 2022 in “bioRxiv (Cold Spring Harbor Laboratory)” The gp130 receptor helps in tissue regeneration and disease progression, and manipulating it could improve healing and prevent disease.
June 2025 in “Medical Science Journal for Advance Research” Higher levels of MIG and IP-10 may help diagnose and monitor Alopecia Areata.
May 2005 in “Molecular Carcinogenesis” mrp/plf-mRNA can indicate tumor-promoting effects in skin.
November 2025 in “The Journal of Immunology” Different γδ T cell types have unique roles in causing alopecia areata.
8 citations
,
February 2015 in “Cellular immunology” Deleting Snai2 and Snai3 causes fatal autoimmunity.
133 citations
,
January 2009 in “Nature” Lgr5 and the vitamin D receptor are key in controlling skin inflammation and tumor risk in mice.
September 2025 in “Diseases” Higher levels of certain proteins in the blood are linked to more severe patchy alopecia areata.
3 citations
,
December 2023 in “Aging” hsa_circ_0002980 can help stop liver cancer cells from growing and spreading.
25 citations
,
November 2017 in “Molecular Medicine Reports” PlncRNA-1 helps hair follicle stem cells grow and develop by controlling a specific cell signaling pathway.
220 citations
,
June 2013 in “The Journal of Pathology” Lichen planopilaris may be an autoimmune disease causing hair loss due to immune system issues in hair follicles.
April 2010 in “Cancer Research” Mcl-1 can activate Wnt signaling in skin cells, promoting growth and possibly cancer.
25 citations
,
May 1994 in “Journal of Investigative Dermatology” Researchers found a new gene, hacl-1, that is active in mouse hair follicles during hair growth and may be important for hair biology.
January 2026 in “Figshare” ASLNC168501 may help restore hair growth in androgenetic alopecia by improving hair follicle stem cell function.
October 2025 in “International Journal of Dermatology” JAK inhibitors may help treat certain types of hair loss, but more research is needed.
April 2021 in “Journal of Investigative Dermatology” Arg1+ macrophages may play a role in causing alopecia areata.
7 citations
,
September 2017 in “Scientific Reports” Mice with too much sPLA₂-IIA have hair loss and poor wound healing due to abnormal hair growth and stem cell depletion.
1 citations
,
September 2004 in “Experimental Dermatology” MC-1R is present in skin cells and may help reduce inflammation.
6 citations
,
October 2017 in “Oncotarget” Hairless mice are more vulnerable to Listeria infection, but gut microbiota can help reduce damage.
1 citations
,
January 2005 in “Experimental Dermatology” MC-1R in skin cells may influence inflammation and collagen production.
Lhx2 helps retinal cells respond to signals for eye development.
July 2024 in “Journal of Investigative Dermatology”
October 2025 in “Clinical Cosmetic and Investigational Dermatology” Targeting specific cell interactions may help treat skin fibrosis.
15 citations
,
May 2016 in “Archives of Dermatological Research” ULBP3 could be a marker for diagnosing alopecia areata incognita and may be linked to its cause and development.
Ubiquitination of the insulin receptor regulates collagen secretion in human skin.
December 2023 in “Communications biology” Targeting the HEDGEHOG-GLI1 pathway could help treat keloids.
May 2023 in “The journal of investigative dermatology/Journal of investigative dermatology” A potential treatment for atopic dermatitis could be to increase PADI1 expression to improve skin barrier function.
March 2018 in “Suez Canal University Medical Journal” New drugs targeting the JAK-STAT pathway show promise for treating inflammatory skin diseases.
333 citations
,
March 2000 in “Proceedings of the National Academy of Sciences” Overexpressing GLI-1 in mice skin can cause tumors like human basal cell carcinomas.
January 2026 in “Figshare” ASLNC168501 may help treat hair loss by boosting hair follicle stem cell activity.