Diabetes impairs wound healing, leading to significant morbidity and mortality. Neutrophils, the primary leukocytes involved in early wound healing, can form extracellular traps (NETs) to combat infections. However, NETs can also cause tissue damage. This study demonstrates that neutrophils from type 1 and type 2 diabetic humans and mice are primed to produce NETs, a process known as NETosis. Elevated expression of peptidylarginine deiminase 4 (PAD4), an enzyme crucial for chromatin decondensation, was observed in diabetic neutrophils. In diabetic mice, NETosis led to delayed wound healing, with higher levels of citrullinated histone H3 (H3Cit), a marker of NETs, in the wounds. Deletion of *Pad4* in mice accelerated wound healing compared to wild-type (WT) mice, and this effect was not compromised by diabetes. DNase 1, which breaks down NETs, accelerated wound healing in both diabetic and normoglycemic WT mice. These findings suggest that NETs impair wound healing, particularly in diabetes, where neutrophils are more susceptible to NETosis. Inhibiting NETosis or cleaving NETs may improve wound healing and reduce chronic inflammation in diabetes.Diabetes impairs wound healing, leading to significant morbidity and mortality. Neutrophils, the primary leukocytes involved in early wound healing, can form extracellular traps (NETs) to combat infections. However, NETs can also cause tissue damage. This study demonstrates that neutrophils from type 1 and type 2 diabetic humans and mice are primed to produce NETs, a process known as NETosis. Elevated expression of peptidylarginine deiminase 4 (PAD4), an enzyme crucial for chromatin decondensation, was observed in diabetic neutrophils. In diabetic mice, NETosis led to delayed wound healing, with higher levels of citrullinated histone H3 (H3Cit), a marker of NETs, in the wounds. Deletion of *Pad4* in mice accelerated wound healing compared to wild-type (WT) mice, and this effect was not compromised by diabetes. DNase 1, which breaks down NETs, accelerated wound healing in both diabetic and normoglycemic WT mice. These findings suggest that NETs impair wound healing, particularly in diabetes, where neutrophils are more susceptible to NETosis. Inhibiting NETosis or cleaving NETs may improve wound healing and reduce chronic inflammation in diabetes.