Selective inhibition of PKR by C16 accelerates diabetic wound healing by inhibiting NALP3 expression in mice
Author:
Funder
Science and Engineering Research Board
Publisher
Springer Science and Business Media LLC
Subject
Pharmacology,Immunology
Link
https://link.springer.com/content/pdf/10.1007/s00011-022-01667-y.pdf
Reference35 articles.
1. Mirza RE, Fang MM, Weinheimer-Haus EM, Ennis WJ, Koh TJ. Sustained inflammasome activity in macrophages impairs wound healing in type 2 diabetic humans and mice. Diabetes. 2014;63:1103–14.
2. Kant V, Gopal A, Pathak NN, Kumar P, Tandan SK, Kumar D. Antioxidant and anti-inflammatory potential of curcumin accelerated the cutaneous wound healing in streptozotocin-induced diabetic rats. Int Immunopharmacol. 2014;20:322–30. https://doi.org/10.1016/j.intimp.2014.03.009.
3. Okonkwo UA, Dipietro LA. Diabetes and wound angiogenesis. Int J Mol Sci. 2017;18:1–15.
4. Mirza RE, Fang MM, Ennis WJ, Kohl TJ. Blocking interleukin-1β induces a healing-associated wound macrophage phenotype and improves healing in type 2 diabetes. Diabetes. 2013;62:2579–87.
5. Weinheimer-Haus EM, Mirza RE, Koh TJ. Nod-like receptor protein-3 inflammasome plays an important role during early stages of wound healing. PLoS ONE. 2015;10:1–13.
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