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@ARTICLE{Khadjeh:151063,
      author       = {Khadjeh, Sara and Hindmarsh, Vanessa and Weber, Frederike
                      and Cyganek, Lukas and Vidal, Ramon O. and Torkieh, Setare
                      and Streckfuss-Bömeke, Katrin and Lbik, Dawid and Tiburcy,
                      Malte and Mohamed, Belal A. and Bonn, Stefan and Toischer,
                      Karl and Hasenfuss, Gerd},
      title        = {{CRISPLD}1: a novel conserved target in the transition to
                      human heart failure},
      journal      = {Basic research in cardiology},
      volume       = {115},
      number       = {3},
      issn         = {0300-8428},
      address      = {Berlin},
      publisher    = {Springer},
      reportid     = {DZNE-2020-01048},
      pages        = {27},
      year         = {2020},
      abstract     = {Heart 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.},
      keywords     = {Amino Acid Sequence / Animals / Aortic Valve Stenosis:
                      complications / Aortic Valve Stenosis: genetics / Aortic
                      Valve Stenosis: metabolism / Apoptosis / Biopsy / Calcium:
                      metabolism / Calcium Signaling / Cell Adhesion Molecules:
                      chemistry / Cell Adhesion Molecules: deficiency / Cell
                      Adhesion Molecules: genetics / Cell Adhesion Molecules:
                      metabolism / Conserved Sequence / Down-Regulation /
                      Evolution, Molecular / Female / Heart Failure: complications
                      / Heart Failure: genetics / Heart Failure: metabolism /
                      Humans / Induced Pluripotent Stem Cells: cytology / Male /
                      Mice / Myocardium: metabolism / Myocytes, Cardiac: cytology
                      / Myocytes, Cardiac: metabolism / Transcriptome /
                      Transforming Growth Factor beta: metabolism},
      cin          = {AG Bonn 1},
      ddc          = {610},
      cid          = {I:(DE-2719)1410003},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC7060963},
      pubmed       = {pmid:32146539},
      doi          = {10.1007/s00395-020-0784-4},
      url          = {https://pub.dzne.de/record/151063},
}