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KLF4 Promotes Diabetic Chronic Wound Healing by Suppressing Th17 Cell Differentiation in an MDSC-Dependent Manner.

Xiong YangBryan J MathisYu HuangWencheng LiYing Shi
Published in: Journal of diabetes research (2021)
Our study revealed a previously unreported function of KLF4-regulated MDSCs in diabetic wound healing and identified APTO-253 as a potential agent to improve the healing of pressure ulcers.
Keyphrases
  • wound healing
  • transcription factor
  • type diabetes
  • single cell
  • climate change