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000151063 1001_ $$00000-0002-0589-4969$$aKhadjeh, Sara$$b0
000151063 245__ $$aCRISPLD1: a novel conserved target in the transition to human heart failure
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000151063 520__ $$aHeart failure is a major health problem worldwide with a significant morbidity and mortality rate. Although studied extensively in animal models, data from patients at the compensated disease stage are lacking. We sampled myocardium biopsies from aortic stenosis patients with compensated hypertrophy and moderate heart failure and used transcriptomics to study the transition to failure. Sequencing and comparative analysis of analogous samples of mice with transverse aortic constriction identified 25 candidate genes with similar regulation in response to pressure overload, reflecting highly conserved molecular processes. The gene cysteine-rich secretory protein LCCL domain containing 1 (CRISPLD1) is upregulated in the transition to failure in human and mouse and its function is unknown. Homology to ion channel regulatory toxins suggests a role in Ca2+ cycling. CRISPR/Cas9-mediated loss-of-function leads to dysregulated Ca2+ handling in human-induced pluripotent stem cell-derived cardiomyocytes. The downregulation of prohypertrophic, proapoptotic and Ca2+-signaling pathways upon CRISPLD1-KO and its upregulation in the transition to failure implicates a contribution to adverse remodeling. These findings provide new pathophysiological data on Ca2+ regulation in the transition to failure and novel candidate genes with promising potential for therapeutic interventions.
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000151063 650_2 $$2MeSH$$aAmino Acid Sequence
000151063 650_2 $$2MeSH$$aAnimals
000151063 650_2 $$2MeSH$$aAortic Valve Stenosis: complications
000151063 650_2 $$2MeSH$$aAortic Valve Stenosis: genetics
000151063 650_2 $$2MeSH$$aAortic Valve Stenosis: metabolism
000151063 650_2 $$2MeSH$$aApoptosis
000151063 650_2 $$2MeSH$$aBiopsy
000151063 650_2 $$2MeSH$$aCalcium: metabolism
000151063 650_2 $$2MeSH$$aCalcium Signaling
000151063 650_2 $$2MeSH$$aCell Adhesion Molecules: chemistry
000151063 650_2 $$2MeSH$$aCell Adhesion Molecules: deficiency
000151063 650_2 $$2MeSH$$aCell Adhesion Molecules: genetics
000151063 650_2 $$2MeSH$$aCell Adhesion Molecules: metabolism
000151063 650_2 $$2MeSH$$aConserved Sequence
000151063 650_2 $$2MeSH$$aDown-Regulation
000151063 650_2 $$2MeSH$$aEvolution, Molecular
000151063 650_2 $$2MeSH$$aFemale
000151063 650_2 $$2MeSH$$aHeart Failure: complications
000151063 650_2 $$2MeSH$$aHeart Failure: genetics
000151063 650_2 $$2MeSH$$aHeart Failure: metabolism
000151063 650_2 $$2MeSH$$aHumans
000151063 650_2 $$2MeSH$$aInduced Pluripotent Stem Cells: cytology
000151063 650_2 $$2MeSH$$aMale
000151063 650_2 $$2MeSH$$aMice
000151063 650_2 $$2MeSH$$aMyocardium: metabolism
000151063 650_2 $$2MeSH$$aMyocytes, Cardiac: cytology
000151063 650_2 $$2MeSH$$aMyocytes, Cardiac: metabolism
000151063 650_2 $$2MeSH$$aTranscriptome
000151063 650_2 $$2MeSH$$aTransforming Growth Factor beta: metabolism
000151063 7001_ $$aHindmarsh, Vanessa$$b1
000151063 7001_ $$aWeber, Frederike$$b2
000151063 7001_ $$aCyganek, Lukas$$b3
000151063 7001_ $$0P:(DE-2719)9000325$$aVidal, Ramon O.$$b4$$udzne
000151063 7001_ $$aTorkieh, Setare$$b5
000151063 7001_ $$aStreckfuss-Bömeke, Katrin$$b6
000151063 7001_ $$aLbik, Dawid$$b7
000151063 7001_ $$aTiburcy, Malte$$b8
000151063 7001_ $$aMohamed, Belal A.$$b9
000151063 7001_ $$0P:(DE-2719)2810547$$aBonn, Stefan$$b10$$udzne
000151063 7001_ $$0P:(DE-HGF)0$$aToischer, Karl$$b11
000151063 7001_ $$aHasenfuss, Gerd$$b12
000151063 77318 $$2Crossref$$3journal-article$$a10.1007/s00395-020-0784-4$$bSpringer Science and Business Media LLC$$d2020-03-07$$n3$$p27$$tBasic Research in Cardiology$$v115$$x0300-8428$$y2020
000151063 773__ $$0PERI:(DE-600)1458470-0$$a10.1007/s00395-020-0784-4$$gVol. 115, no. 3, p. 27$$n3$$p27$$tBasic research in cardiology$$v115$$x0300-8428$$y2020
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