Research Highlight

Wound healer

doi:10.1038/nindia.2011.133 Published online 22 September 2011

Researchers have found that the neurotransmitter dopamine by acting through its D2 receptors can regulate wound healing by inhibiting the formation of new blood vessels (angiogenesis) in wound tissues.

The research assumes importance since dopamine D2 receptor antagonists are already used in clinics for other purposes and could be effectively employed as an inexpensive drug for the management of wounds.

The physiological process of wound healing is made up of different phases. Angiogenesis or formation of new blood vessels is an important phase. The skin is richly supplied by sympathetic nerves, which have been reported to play a significant role in cutaneous wound healing. Dopamine (DA) is an important neurotransmitter released by the sympathetic nerve endings. Recent studies have demonstrated the potent anti-angiogenic action of DA, which is mediated through its D2 DA receptors.

The researchers postulated that dopamine may have a role in formation of new blood vessels in dermal wound tissues and subsequently in the process of wound healing. They studied the therapeutic efficacy of D2 DA receptor antagonists for faster wound healing in mice.

They found that treatment with specific D2 DA receptor antagonists significantly enhanced the process of dermal wound healing by triggering angiogenesis in wound tissues. The reason behind this was the increase in a transcription factor HoxD3 and its target a5b1 integrin, which play a pivotal role in angiogenesis.

The results could have significant translational value from the bench to the bedside for efficient wound management, the researchers say.

Authors of this work are from: Department of Signal Transduction and Biogenic Amines, Chittaranjan National Cancer Institute, Kolkata, India and Department of Pathology, The Ohio State University, Columbus, Ohio, United States of America.


  1. Shome, S. et al. Dopamine Regulates Angiogenesis in Normal Dermal Wound Tissues. Plos. ONE. 6, e25215. doi: 10.1371/journal.pone.0025215 (2011) | Article |