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A review of KLF4 and inflammatory disease: Current status and future perspective

Yidan Liang1, Jiamin Zhao1, Tengkun Dai1

  • 1Special Key Laboratory of Gene Detection &Therapy of Guizhou Province, Zunyi Medical University, Zunyi, Guizhou 563000, China; Department of Immunology, Zunyi Medical University, Zunyi, Guizhou 563000, China.

Pharmacological Research
|August 12, 2024
PubMed

Insights

Krüppel-like factor 4 (KLF4) is a key regulator in inflammation, impacting numerous diseases. Understanding KLF4

Area of Science:

  • Molecular Biology
  • Immunology
  • Genetics

Background:

  • Inflammation is a critical biological response implicated in numerous diseases.
  • Krüppel-like transcription factors (KLFs) are crucial regulators of cellular processes.
  • KLF4, a member of the KLF family, possesses dual transcriptional regulatory functions.

Purpose of the Study:

  • To systematically review the molecular regulatory network of KLF4 in inflammatory diseases.
  • To elucidate the specific functions and mechanisms of KLF4 in pathogenesis.
  • To highlight KLF4 as a potential therapeutic target for inflammatory conditions.

Main Methods:

  • Systematic literature review of studies on KLF4 and inflammation.
  • Analysis of molecular mechanisms underlying KLF4's role in various inflammatory disorders.
  • Generalization of KLF4's regulatory network and biological functions.

Main Results:

  • KLF4 plays a pivotal role in the pathogenesis of diverse inflammatory diseases.
  • Evidence links KLF4 to inflammatory bowel disease, osteoarthritis, renal inflammation, pneumonia, and neuroinflammation.
  • KLF4 exhibits complex regulatory functions involving both transcriptional activation and inhibition.

Conclusions:

  • KLF4 is a significant factor in the development and progression of inflammatory diseases.
  • Targeting KLF4 offers promising therapeutic strategies for managing inflammation.
  • Further research into KLF4's biological functions can yield novel intervention approaches.
Keywords:
Expression regulation mechanismInflammatory diseasesKLF4

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