Decoding the Kruppel-like Transcription Factors in Atherosclerosis: Insight from Molecular and Translational...

Area of Science:

• Cardiovascular Research
• Molecular Biology
• Translational Medicine

Background:

• Atherosclerosis is a major cause of cardiovascular and cerebrovascular diseases, driven by inflammation, lipid issues, and vascular remodeling.
• Current treatments like lifestyle changes and statins have limitations, with high mortality and morbidity rates persisting.
• Kruppel-like factors (KLFs) are crucial transcription factors influencing numerous physiological and pathological processes.

Purpose of the Study:

• To construct a comprehensive network illustrating the role of KLFs in atherosclerosis pathogenesis.
• To identify novel therapeutic substances and approaches targeting KLF-modulated pathways for atherosclerosis.
• To explore gene therapy and nanotechnology for precision medicine in atherosclerotic cardiovascular disease.

Main Methods:

• Literature review focusing on the molecular mechanisms of KLFs in atherosclerosis.
• Network construction to map KLF interactions in atherosclerotic lesion development.
• Analysis of emerging therapeutic strategies, including gene therapy and nanotechnology.

Main Results:

• Specific KLF family members (KLF2, KLF4, KLF5, KLF6, KLF14) are pivotal in regulating endothelial homeostasis, smooth muscle cell changes, and inflammation.
• Novel substances targeting KLF pathways show potential in attenuating atherosclerosis.
• Gene therapy and nanotechnology present emerging approaches for KLF-modulated treatment.

Conclusions:

• KLFs play a central role in the initiation and progression of atherosclerotic lesions.
• Targeting KLF pathways offers new therapeutic avenues for atherosclerotic cardiovascular disease.
• This review highlights the translational and precision medicine potential of KLF modulation.