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Vascular Fibrosis and Disease

  • Mengxue Zhang
  • Bowen Wang
  • K. Craig Kent
  • Lian-Wang Guo
Chapter
Part of the Molecular and Translational Medicine book series (MOLEMED)

Abstract

Fibrosis can lead to a broad range of diseases affecting essentially every organ. Thus, interventions targeting fibrosis are expected to have profound therapeutic effects. However, thus far there are no effective clinical treatments to specifically block fibrotic processes, underscoring the necessity of enhanced research efforts in this arena. The hallmark of vascular fibrotic disorders is extensive extracellular matrix remodeling primarily mediated by myofibroblasts. A prominent feature of the vasculature is that all three major constituent cell types, fibroblasts, smooth muscle cells, and endothelial cells, maintain phenotypic plasticity. In response to various fibrogenic stimuli, these vascular cells along with progenitor cells can transform into myofibroblasts or myofibroblast-like cells, collectively yet variably contributing to vascular fibrosis. As such, the vascular system provides useful models for studying fibrotic mechanisms. In this chapter, we focus on vascular fibrosis and associated diseases, providing an overview of the underlying cellular and molecular mechanisms and their multifaceted impacts on disease outcomes. Potential antifibrotic targets and the emerging importance of epigenetic regulators in the major vascular diseases are also discussed.

Keywords

Vascular fibrosis Atherosclerosis Restenosis Arterial stiffness Myofibroblast Extracellular matrix TGFbeta Epigenetic regulators 

Notes

Acknowledgments

This work was supported by NIH grants R01 HL133665 (to L-WG), R01HL143469 and R01HL129785 (both to KCK and L-WG), and R01HL-068673 (to KCK), and AHA predoctoral fellowship awards (17PRE33670865 to MZ and 16PRE30160010 to BW).

We thank Dr. Matthew Stratton in the Davis Heart and Lung Research Institute of the Ohio State University for informative discussion and proofreading.

Conflict of Interest

The authors declare no conflict of interest.

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Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  • Mengxue Zhang
    • 1
  • Bowen Wang
    • 1
    • 2
  • K. Craig Kent
    • 2
  • Lian-Wang Guo
    • 1
    • 2
    • 3
  1. 1.Davis Heart and Lung Research Institute, Wexner Medical CenterThe Ohio State UniversityColumbusUSA
  2. 2.Department of Surgery, College of MedicineThe Ohio State UniversityColumbusUSA
  3. 3.Department of Physiology and Cell Biology, College of MedicineThe Ohio State UniversityColumbusUSA

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