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Atherosclerotic disease

Saving KLF2/4 from γ-protocadherin to reduce vascular inflammation and atherosclerosis

Nature Cardiovascular Research volume 3, pages 1021–1023 (2024)Cite this article

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Atherosclerosis occurs in arterial regions exposed to disturbed flow, where endothelial expression of flow-sensitive, atheroprotective genes such as KLF2 and KLF4 is reduced. Protecting the endothelial expression of KLF2 and KLF4 from inhibitory factors could be a therapeutic approach to prevent vascular inflammation and atherosclerosis.

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Fig. 1: Flow-dependent activation of KLF2/4 pathway and the role and mechanisms of PCDHG in atherosclerosis.

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Acknowledgements

This work was supported by funding from US National Institutes of Health (NIH) grants HL119798, HL139757 and HL151358 to H.J. H.J. was also supported by a Wallace H. Coulter distinguished faculty chair endowment. C.P. was supported by NIH grant T32HL166146. K.B. was supported by NIH grants T32HL007745 and F32HL167625.

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Authors and Affiliations

  1. Wallace H. Coulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA, USA

    Christian Park, Kyung In Baek & Hanjoong Jo

  2. Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA, USA

    Hanjoong Jo

Authors
  1. Christian Park
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  2. Kyung In Baek
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  3. Hanjoong Jo
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Correspondence to Hanjoong Jo.

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Competing interests

H.J. is the founder of Flokines Pharma, established to develop anti-atherosclerotic therapeutics by targeting flow-sensitive genes, but has no relationship to the work reported by Joshi et al.4. All other authors report no conflicts of interest.

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Park, C., Baek, K.I. & Jo, H. Saving KLF2/4 from γ-protocadherin to reduce vascular inflammation and atherosclerosis. Nat Cardiovasc Res 3, 1021–1023 (2024). https://doi.org/10.1038/s44161-024-00523-y

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