Detection of macrophages engulfing cholesterol crystals and docosahexaenoic acid from spontaneous ruptured aortic plaque


      We visualized macrophages engulfing cholesterol crystals from spontaneously ruptured aortic plaques sampled by angioscopy. Docosahexaenoic acid cholesterol ester (DHA-CE) was demonstrated by imaging mass spectrometry. DHA-CE is reported to be produced by macrophages against inflammation. Activities of macrophages against atherosclerosis inside plaques was shown from spontaneously ruptured aortic plaques in situ.

      Learning objectives

      Activities of macrophages such as engulfing cholesterol crystals and producing docosahexaenoic acid cholesterol ester were shown from spontaneously ruptured aortic plaques in situ.


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        • Poznyak A.V.
        • Nikiforov N.G.
        • Markin A.M.
        • Kashirskikh D.A.
        • Myasoedova V.A.
        • Gerasimova E.V.
        • Orekhov A.N.
        Overview of OxLDL and its impact on cardiovascular health: focus on atherosclerosis.
        Front. Pharmacol. 2021; 11613780
        • Komatsu S.
        • Yutani C.
        • Ohara T.
        • Takahashi S.
        • Takewa M.
        • Hirayama A.
        • Kodama K.
        Angioscopic evaluation of spontaneously ruptured aortic plaques.
        J. Am. Coll. Cardiol. 2018; 71: 2893-2902
        • Iwa N.
        • Yutani C.
        • Komatsu S.
        • Takahashi S.
        • Takewa M.
        • Ohara T.
        • et al.
        Novel methods for detecting human cholesterol crystals from sampled blood.
        Lab. Med. 2022; 53: 255-261
        • Komatsu S.
        • Yutani C.
        • Takahashi S.
        • Takewa M.
        • Ohara T.
        • Hirayama A.
        • Kodama K.
        Debris collected in-situ from spontaneously ruptured atherosclerotic plaque invariably contains large cholesterol crystals and evidence of activation of innate inflammation: insights from non-obstructive general angioscopy.
        Atherosclerosis. 2022; 352: 96-102
        • Thacker S.G.
        • Zarzour A.
        • Chen Y.
        • Alcicek M.S.
        • Freeman L.A.
        • Sviridov D.O.
        • et al.
        High-density lipoprotein reduces inflammation from cholesterol crystals by inhibiting inflammasome activation.
        Immunology. 2016; 149: 306-319
        • Zaima N.
        • Sasaki T.
        • Tanaka H.
        • Cheng X.W.
        • Onoue K.
        • Hayasaka T.
        • Goto-Inoue N.
        • Enomoto H.
        • Unno N.
        • Kuzuya M.
        • Setou M.
        Imaging mass spectrometry-based histopathologic examination of atherosclerotic lesions.
        Atherosclerosis. 2011; 217: 27-32
        • Mulay S.R.
        • Anders H.J.
        N. Engl. J. Med. 2016; 23: 2465-2476
        • Nidorf S.M.
        • Fiolet A.
        • Abela G.S.
        Viewing atherosclerosis through a crystal lens: how the evolving structure of cholesterol crystals in atherosclerotic plaque alters its stability.
        J. Clin. Lipidol. 2020; 14: 619-630
        • Barrett J.T.
        Macrophages in atherosclerosis regression.
        Arterioscler. Thromb. Vasc. Biol. 2020; 40: 20-33
        • Oishi Y.
        • Spann N.J.
        • Link V.M.
        • Muse E.D.
        • Strid T.
        • Edillor C.
        • Kolar M.J.
        • Matsuzaka T.
        • Hayakawa S.
        • Tao J.
        • Kaikkonen M.U.
        • Carlin A.F.
        • Lam M.T.
        • Manabe I.
        • Shimano H.
        • et al.
        SREBP1 contributes to resolution of pro-inflammatory TLR4 signaling by reprogramming fatty acid metabolism.
        Cell Metab. 2017; 25: 412-427