Complementary roles of mechanotransduction and inflammation in vascular homeostasis

Marcos Latorre, Bart Spronck, Jay D. Humphrey*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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Abstract

Arteries are exposed to relentless pulsatile haemodynamic loads, but via mechanical homeostasis they tend to maintain near optimal structure, properties and function over long periods in maturity in health. Numerous insults can compromise such homeostatic tendencies, however, resulting in maladaptations or disease. Chronic inflammation can be counted among the detrimental insults experienced by arteries, yet inflammation can also play important homeostatic roles. In this paper, we present a new theoretical model of complementary mechanobiological and immunobiological control of vascular geometry and composition, and thus properties and function. We motivate and illustrate the model using data for aortic remodelling in a common mouse model of induced hypertension. Predictions match the available data well, noting a need for increased data for further parameter refinement. The overall approach and conclusions are general, however, and help to unify two previously disparate literatures, thus leading to deeper insight into the separate and overlapping roles of mechanobiology and immunobiology in vascular health and disease.

Original languageEnglish
Article number20200622
Number of pages20
JournalProceedings of the Royal Society A-Mathematical Physical and Engineering Sciences
Volume477
Issue number2245
DOIs
Publication statusPublished - 27 Jan 2021

Keywords

  • hypertension
  • inflammation
  • homeostasis
  • mechanotransduction
  • artery
  • SMOOTH-MUSCLE-CELLS
  • AORTIC ADVENTITIAL FIBROBLASTS
  • ANGIOTENSIN-II
  • COLLAGEN-SYNTHESIS
  • HYPERTENSION
  • TISSUE
  • ACTIVATION
  • WALL
  • MACROPHAGES
  • RECEPTOR

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