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Diverse mechanisms of KLFs in skeletal diseases and their clinical potentials

ChunYang Han1, Jian Xu2, Hang Yu2

  • 1Department of Stomatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China; Hubei Province Key Laboratory of Oral and Maxillofacial Development and Regeneration, Wuhan, 430022, China; The First Clinical College, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Biochemical and Biophysical Research Communications
|November 13, 2025
PubMed

Insights

Krüppel-like factors (KLFs) are key proteins regulating bone health and disease. Understanding their role in skeletal disorders offers new diagnostic and therapeutic precision medicine strategies.

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Krüppel-like factors (KLFs) are zinc finger DNA-binding proteins crucial for skeletal development and pathogenesis.
  • KLFs regulate diverse cellular activities like proliferation, differentiation, apoptosis, and autophagy via gene transcription.
  • Aberrant KLF expression is linked to skeletal disorders including osteoporosis, impaired fracture healing, osteoarthritis (OA), and bone tumors.

Purpose of the Study:

  • To review the regulatory mechanisms of KLFs in major skeletal pathologies.
  • To focus on KLF functions in osteoblasts, osteoclasts, and chondrocytes.
  • To explore the clinical potential of KLFs as diagnostic biomarkers and therapeutic targets.

Main Methods:

  • Literature review and synthesis of current knowledge on KLFs in skeletal diseases.
  • Analysis of KLF roles in specific bone cell types (osteoblasts, osteoclasts, chondrocytes).
  • Evaluation of KLF potential in diagnostics and drug development for skeletal conditions.

Main Results:

  • KLFs are implicated in the pathogenesis of various skeletal disorders.
  • KLFs exhibit critical functions in key skeletal cell types.
  • KLFs show promise as biomarkers for early diagnosis and as therapeutic targets.

Conclusions:

  • KLFs are vital regulators in skeletal development and disease.
  • Targeting KLFs presents opportunities for precision medicine in skeletal diseases.
  • Further research into KLF molecular mechanisms is needed for clinical translation.

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