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. 2021 Sep 13;16(9):e0257175. doi: 10.1371/journal.pone.0257175

Fig 7. LIPUS ameliorates DES-induced coronary adventitial inflammation and resultant coronary hyperconstricting responses in pigs in vivo.

Fig 7

DES implantation induces coronary adventitial and PVAT inflammatory changes, including adventitial vasa vasorum augmentation, Mφ infiltration, and cytokine expressions in pigs in vivo. Importantly, cardiac lymphatic vessels act as a drainage for inflammatory changes, and thus impaired lymphatic function exacerbates adventitial inflammation, and subsequent medial VSMC hypercontraction through Rho-kinase activation (a central molecular switch of coronary artery spasm). In the present study, we were able to demonstrate that the LIPUS therapy enhanced coronary lymph-angiogenesis through up-regulations of eNOS and VEGF-C/VEGFR3, which prompted lymph transport speed for inflammatory cells (Mφ) and inflammatory cytokines (IL-1β). Mechanistically, the LIPUS therapy suppressed Rho-kinase activation and subsequent medial VSMC hypercontraction. DES = drug-eluting stent; Mφ = macrophage; PVAT = perivascular adipose tissue; VSMC = vascular smooth muscle cell; other abbreviations as in Figs 1–4.