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000291568 1001_ $$aMueller, Karin Anne Lydia$$b0
000291568 245__ $$aMacrophage Migration Inhibitory Factor Promotes Thromboinflammation and Predicts Fast Progression of Aortic Stenosis.
000291568 260__ $$aStanford, Calif.$$bHighWire$$c2024
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000291568 500__ $$a#LA:D431# / 2024 Sep;44(9):2118-2135
000291568 520__ $$aAortic stenosis (AS) is driven by progressive inflammatory and fibrocalcific processes regulated by circulating inflammatory and valve resident endothelial and interstitial cells. The impact of platelets, platelet-derived mediators, and platelet-monocyte interactions on the acceleration of local valvular inflammation and mineralization is presently unknown.We prospectively enrolled 475 consecutive patients with severe symptomatic AS undergoing aortic valve replacement. Clinical workup included repetitive echocardiography, analysis of platelets, monocytes, chemokine profiling, aortic valve tissue samples for immunohistochemistry, and gene expression analysis.The patients were classified as fast-progressive AS by the median ∆Vmax of 0.45 m/s per year determined by echocardiography. Immunohistological aortic valve analysis revealed enhanced cellularity in fast-progressive AS (slow- versus fast-progressive AS; median [interquartile range], 247 [142.3-504] versus 717.5 [360.5-1234]; P<0.001) with less calcification (calcification area, mm2: 33.74 [27.82-41.86] versus 20.54 [13.52-33.41]; P<0.001). MIF (macrophage migration inhibitory factor)-associated gene expression was significantly enhanced in fast-progressive AS accompanied by significantly elevated MIF plasma levels (mean±SEM; 6877±379.1 versus 9959±749.1; P<0.001), increased platelet activation, and decreased intracellular MIF expression indicating enhanced MIF release upon platelet activation (CD62P, %: median [interquartile range], 16.8 [11.58-23.8] versus 20.55 [12.48-32.28], P=0.005; MIF, %: 4.85 [1.48-9.75] versus 2.3 [0.78-5.9], P<0.001). Regression analysis confirmed that MIF-associated biomarkers are strongly associated with an accelerated course of AS.Our findings suggest a key role for platelet-derived MIF and its interplay with circulating and valve resident monocytes/macrophages in local and systemic thromboinflammation during accelerated AS. MIF-based biomarkers predict an accelerated course of AS and represent a novel pharmacological target to attenuate progression of AS.
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000291568 650_7 $$2Other$$aaortic valve stenosis
000291568 650_7 $$2Other$$abiomarkers
000291568 650_7 $$2Other$$ablood platelets
000291568 650_7 $$2Other$$achemokines
000291568 650_7 $$2Other$$ainflammation
000291568 7001_ $$aLangnau, Carolin$$b1
000291568 7001_ $$00000-0002-6121-2694$$aHarm, Tobias$$b2
000291568 7001_ $$00000-0001-8954-4810$$aSigle, Manuel$$b3
000291568 7001_ $$00000-0002-3223-6857$$aMott, Kristina$$b4
000291568 7001_ $$00000-0001-5807-7615$$aDroppa, Michal$$b5
000291568 7001_ $$00000-0003-4002-4085$$aBorst, Oliver$$b6
000291568 7001_ $$00000-0001-5469-3648$$aRohlfing, Anne-Katrin$$b7
000291568 7001_ $$aGekeler, Sarah$$b8
000291568 7001_ $$0P:(DE-He78)b676990c2f64e3295740d42e356fb053$$aGünter, Manina$$b9$$udkfz
000291568 7001_ $$00000-0002-7692-3480$$aGoebel, Nora$$b10
000291568 7001_ $$aFranke, Ulrich F W$$b11
000291568 7001_ $$aRadwan, Medhat$$b12
000291568 7001_ $$00000-0001-8649-597X$$aSchlensak, Christian$$b13
000291568 7001_ $$00000-0002-6497-6972$$aJanning, Henrik$$b14
000291568 7001_ $$aScheuermann, Sophia$$b15
000291568 7001_ $$aSeitz, Christian M$$b16
000291568 7001_ $$00000-0002-5008-2572$$aRath, Dominik$$b17
000291568 7001_ $$aKreisselmeier, Klaus-Peter$$b18
000291568 7001_ $$aCastor, Tatsiana$$b19
000291568 7001_ $$aMueller, Iris Irmgard$$b20
000291568 7001_ $$aSchulze, Harald$$b21
000291568 7001_ $$0P:(DE-He78)d3dbba28fe1239effd15962787cbc363$$aAutenrieth, Stella$$b22$$eLast author$$udkfz
000291568 7001_ $$00000-0003-1124-9592$$aGawaz, Meinrad Paul$$b23
000291568 773__ $$0PERI:(DE-600)1494427-3$$a10.1161/ATVBAHA.124.321000$$gp. ATVBAHA.124.321000$$n9$$p2118-2135$$tArteriosclerosis, thrombosis, and vascular biology$$v44$$x0276-5047$$y2024
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