Konstantin Kahnert
3 Papers
Konstantin Kahnert is an academic researcher. The author has co-authored 1 publications.
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Papers
Outlining cardiac ion channel protein interactors and their signature in the human electrocardiogram
Svetlana Rajkumar Maurya,Robert W. Mills,Konstantin Kahnert,David Y. Chiang,Pia R. Lundegaard,Mingliang Zhang,Eli Rothenberg,Alfred L. George,Calum A. MacRae,Mario Delmar,Alicia Lundby +10 more
TL;DR: The experimental identification of the ensemble of protein interactors for 13 types of ion channels in murine cardiac tissue is reported, and a computational framework to reconstruct human cardiomyocyte ion channel networks from deep proteome mapping of human heart tissue and human heart single-cell gene expression data is established.
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Proteomics couples electrical remodelling to inflammation in a murine model of heart failure with sinus node dysfunction.
Konstantin Kahnert,Luca Soattin,Robert W Mills,Claire Wilson,Svetlana Maurya,Andrea Sorrentino,Sami Al-Othman,Roman Tikhomirov,Yordi J. van de Vegte,Finn B Hansen,Jonathan Achter,Wei Hu,Min Zi,Matthew Smith,P. Van der Harst,Morten S Olesen,Kristine Boisen Olsen,Jytte Banner,Thomas H L Jensen,Henggui Zhang,Mark R. Boyett,Alicia D'Souza,Alicia Lundby +22 more
TL;DR: The protein and phosphorylation remodeling of SND in heart failure is outlined, a role for inflammation in electrophysiological remodelling of the sinus node is highlighted, and galectin-3 signalling is presented as a target to ameliorate SND in heart failure.
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An unbiased molecular characterisation of peripartum cardiomyopathy hearts identifies mast cell chymase as a new diagnostic candidate.
J. Mulvey,C. Sailer,J.S. Achter,Gregory N. Milburn,R.C. Bretherton,Konstantin Kahnert,S. Erbil Bilir,H. Hvid,C. Pyke,F. Gustafsson,L. Adamo,K. Campbell,K. Herum,A. Lundby +13 more
Abstract: Peripartum cardiomyopathy (PPCM) is a rare form of acute heart failure that develops in women toward the end of pregnancy or early postpartum. No effective, specific treatment for PPCM is available and heart transplantation or mechanical circulatory support may be required in severe cases where drug treatment for heart failure is insufficient. The mechanisms through which the disease progresses are not well understood, and despite similar clinical characteristics to dilated cardiomyopathy of other etiologies (nonperipartum cardiomyopathy; NPCM) it is not known how the molecular remodeling differs between these groups. We aimed to provide insight into the human PPCM heart using unbiased methodologies, and to use changes occurring within the heart tissue to facilitate biomarker discovery. We obtained heart tissue from female patients with end-stage disease receiving either heart transplantation or left ventricular assist device implantation, or from organ donors without heart disease as a control group. We performed deep proteomics, single nucleus transcriptomics and spatial transcriptomics, providing a comprehensive map of the molecular phenotype in advanced PPCM compared to both control and NPCM hearts. Consistent with similarities in the clinical phenotypes of PPCM and NPCM, we observed regulation of canonical markers of end-stage heart failure in both PPCM and NPCM hearts in comparison to controls. Among the changes specific to PPCM and that were consistently observed across multiple data types and cohorts was an upregulation of chymase and carboxypeptidase A3, consistent with mast cell proliferation/activation. Analysis of the proteome of peripheral blood serum from a larger cohort of patients with PPCM and controls showed that chymase was strongly predictive of cardiomyopathy in peripartum women. PPCM heart tissue is characterized by increased mast cell proteins chymase and carboxypeptidase A3. Chymase may have clinical utility as a biomarker for the diagnosis of cardiomyopathy in peripartum women.