Aging-associated decline in vascular smooth muscle cell mechanosensation is mediated by Piezo1 channel

Ngoc Luu, Apratim Bajpai, Rui Li, Seojin Park, Mahad Noor, Xiao Ma, Weiqiang Chen

Research output: Contribution to journalArticlepeer-review


Aging of the vasculature is associated with detrimental changes in vascular smooth muscle cell (VSMC) mechanosensitivity to extrinsic forces in their surrounding microenvironment. However, how chronological aging alters VSMCs' ability to sense and adapt to mechanical perturbations remains unexplored. Here, we show defective VSMC mechanosensation in aging measured with ultrasound tweezers-based micromechanical system, force instantaneous frequency spectrum, and transcriptome analyses. The study reveals that aged VSMCs adapt to a relatively inert mechanobiological state with altered actin cytoskeletal integrity, resulting in an impairment in their mechanosensitivity and dynamic mechanoresponse to mechanical perturbations. The aging-associated decline in mechanosensation behaviors is mediated by hyperactivity of Piezo1-dependent calcium signaling. Inhibition of Piezo1 alleviates vascular aging and partially restores the loss in dynamic contractile properties in aged cells. Altogether, our study reveals the signaling pathway underlying aging-associated aberrant mechanosensation in VSMC and identifies Piezo1 as a potential therapeutic mechanobiological target to alleviate vascular aging.

Original languageEnglish (US)
Article numbere14036
JournalAging cell
Issue number2
StatePublished - Feb 2024


  • aging
  • calcium
  • cellular senescence
  • cytoskeleton
  • mechanobiology
  • smooth muscle cells
  • vascular smooth muscle

ASJC Scopus subject areas

  • Aging
  • Cell Biology


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