IL-17A is increased in diabetic wounds and impairs keratinocyte function via histone demethylase JMJD3
Jadie Y. Moon, Sonya J. Wolf, Amrita D. Joshi, He Zhang, James Shadiow, Tyler M. Bauer, Kevin D. Mangum, Lindsey D. Hughes, Christopher O. Audu, William J. Melvin, Emily C. Barrett, Sabrina Rocco, Gabriela Saldana de Jimenez, Amber L. Estor, Moses Nelapudi, Qinmengge Li, Rachael Bogle, Benjamin Levi · 2025
Read IL-17A is increased in diabetic wounds and impairs keratinocyte function via histone demethylase JMJD3 by Jadie Y. Moon, Sonya J. Wolf, Amrita D. Joshi, He Zhang, James Shadiow, Tyler M. Bauer, Kevin D. Mangum, Lindsey D. Hughes, Christopher O. Audu, William J. Melvin, Emily C. Barrett, Sabrina Rocco, Gabriela Saldana de Jimenez, Amber L. Estor, Moses Nelapudi, Qinmengge Li, Rachael Bogle, Benjamin Levi (2025) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/pmc-12824406.txt.
Description
Jadie Moon and co-authors trace how an immune signal slows healing in diabetic wounds. Their 2025 study focuses on keratinocytes, the skin cells that must crawl to close a wound. In type 2 diabetes those cells move poorly and stir excess inflammation.
The signal IL-17A runs high in diabetic wounds. It switches on an enzyme that strips repressive marks from gene switches. The opened genes then block cell movement and feed inflammation. Removing the signal or the enzyme in diabetic mice sped healing and quieted those genes. Human wounds showed the same raised pattern. The authors name the pair as a drug target.
Catalog record
| CREATOR | Jadie Y. Moon, Sonya J. Wolf, Amrita D. Joshi, He Zhang, James Shadiow, Tyler M. Bauer, Kevin D. Mangum, Lindsey D. Hughes, Christopher O. Audu, William J. Melvin, Emily C. Barrett, Sabrina Rocco, Gabriela Saldana de Jimenez, Amber L. Estor, Moses Nelapudi, Qinmengge Li, Rachael Bogle, Benjamin Levi |
|---|---|
| YEAR | 2025 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 99 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |