Cardiac hypertrophy articles within Nature Communications

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  • Article
    | Open Access

    Changes of left ventricular structure are used to predict morbidity and mortality in cardiovascular diseases. Here the authors conducted a study using advanced deep learning technology to analyze left ventricular regional wall thickness (LVRWT) in a large population, identifying 72 significant genetic loci linked to LVRWT traits.

    • Caibo Ning
    • , Linyun Fan
    •  & Xiaoping Miao

  • Article
    | Open Access

    The anti-apoptotic function of Bcl-xL in the heart is diminished by Mst1-mediated phosphorylation of Serine14. Here, the authors show that the Bcl-xL phosphorylation is also promoted by hemodynamic stress, which plays an essential role in mediating compensatory cardiac hypertrophy and contractility.

    • Michinari Nakamura
    • , Mariko Aoyagi Keller
    •  & Junichi Sadoshima

  • Article
    | Open Access

    α1-adrenergic receptors (α1- AR) play critical roles in the cardiovascular and nervous systems. Here, the authors report molecular insights into the mechanisms underlying the discrimination between α1A-AR and α1B-AR by the agonist A61603.

    • Minfei Su
    • , Jinan Wang
    •  & Xin-Yun Huang

  • Article
    | Open Access

    In this study, Hsu et al. show that inhibition of CDK7/12/13 attenuates maladaptive transcriptional activation in cultured cardiomyocytes and a mouse model of heart failure, suggesting that targeting the transcription machinery might be a therapeutic approach to treat heart failure with reduced ejection fraction.

    • Austin Hsu
    • , Qiming Duan
    •  & Saptarsi M. Haldar

  • Article
    | Open Access

    The cardiac vascular niche is of major importance in homeostasis and disease, but knowledge of its complexity in response to injury remains limited. Here we combine lineage tracing with single cell RNA sequencing to show alterations in fibroblasts, endothelial and mural cells in hypertrophic remodeling.

    • Fabian Peisker
    • , Maurice Halder
    •  & Rafael Kramann

  • Article
    | Open Access

    Long noncoding RNAs (lncRNAs) have been shown to play a role in cardiac physiology and disease. Here the authors identify the lncRNA Caren as a cytoplasmic RNA that decreases the translation of a distant gene encoding Hint1, thereby maintaining cardiomyocyte function due to inactivation of the DNA damage response and activation of mitochondrial bioenergetics.

    • Michio Sato
    • , Tsuyoshi Kadomatsu
    •  & Yuichi Oike

  • Article
    | Open Access

    Systemic modulation of branched-chain keto acid (BCKA) metabolism alters cardiac health. Here, the authors define the major fates of BCKA in the heart and demonstrate that acute exposure to BCKA levels found in obesity activates cardiac protein synthesis and markedly alters the heart phosphoproteome.

    • Jacquelyn M. Walejko
    • , Bridgette A. Christopher
    •  & Robert W. McGarrah

  • Article
    | Open Access

    New contractile units are required during cardiac hypertrophy, though it remains unclear precisely where and how these new sarcomeres are added. Here the authors reveal that in the heart, microtubules spatiotemporally regulate mRNAs and ribosomes to build new sarcomeres, a role which is essential for growth.

    • Emily A. Scarborough
    • , Keita Uchida
    •  & Benjamin L. Prosser

  • Article
    | Open Access

    Understanding patient-specific pathobiological pathways is a critical step for advancing precision medicine. Here the authors show that individualized protein-protein interaction networks provide key insight on patient-level pathobiology and clinically relevant pathophenotypic characteristics in a complex disease.

    • Bradley A. Maron
    • , Rui-Sheng Wang
    •  & Joseph Loscalzo

  • Article
    | Open Access

    miR-132 was shown to drive pathological cardiac remodeling, a hallmark of heart failure. Here, the authors show that an antisense inhibitor of miR-132 has favourable pharmacokinetics, safety-tolerability and preclinical efficacy in mouse and porcine models of heart failure.

    • Ariana Foinquinos
    • , Sandor Batkai
    •  & Thomas Thum

  • Article
    | Open Access

    Mutations in Ftkn cause Fukuyama muscular dystrophy, and heart failure is the main cause of death in thes patients. Here the authors show that acute elimination of Fktn in adult mice causes early mortality, and this is associated with myocyte dysfunction, with disorganised Golg-microtubule networks, and that the pathology can be ameliorated with colchicine treatment.

    • Yoshihiro Ujihara
    • , Motoi Kanagawa
    •  & Yuki Katanosaka

  • Article
    | Open Access

    The mechanisms that regulate the activity of Ca2 +/calmodulin-dependent protein kinase II (CaMKII) in the context of heart failure are incompletely understood. Here the authors show that protein arginine methyltransferase 1 (PRMT1) prevents cardiac hyperactivation of CaMKII and heart failure development by methylating CaMKII at arginine residues 9 and 275.

    • Jung-Hoon Pyun
    • , Hyun-Ji Kim
    •  & Jong-Sun Kang

  • Article
    | Open Access

    A small percentage of cardiomyocytes (CM) are of neural crest origin but the function of such cells in the adult zebrafish is unclear. Here, the authors identify this CM subpopulation as expressing the Notch ligand jag2b and if deleted in the embryo, cause severe hypertrophic cardiomyopathy in adulthood.

    • Sarah Abdul-Wajid
    • , Bradley L. Demarest
    •  & H. Joseph Yost

  • Article
    | Open Access

    The mechanisms underlying the transition from cardiac hypertrophy to heart failure following pressure overload are incompletely understood. Here the authors identify the gene programs encoding the morphological and functional characteristics of cardiomyocytes during the transition from early hypertrophy to heart failure via single-cell transcriptomics, establishing a key role for p53 signalling.

    • Seitaro Nomura
    • , Masahiro Satoh
    •  & Issei Komuro

  • Article
    | Open Access

    Common genetic variants in structural proteins contribute to risk of atrial fibrillation (AF). Here, using whole-exome sequencing, the authors identify rare truncating variants in TTN that associate with familial and early-onset AF and show defects in cardiac sarcomere assembly in ttn.2-mutant zebrafish.

    • Gustav Ahlberg
    • , Lena Refsgaard
    •  & Morten S. Olesen

  • Article
    | Open Access

    Hypertrophic cardiomyopathy (HCM) is caused by point mutations in sarcomeric proteins. Here the authors develop an optimized model of the sequestered state of cardiac myosin and define the features affecting the lever arm compliance, allowing them to group mutations in classes and to elucidate the molecular mechanisms leading to cardiac dysfunction in HCM.

    • Julien Robert-Paganin
    • , Daniel Auguin
    •  & Anne Houdusse

  • Article
    | Open Access

    Hypertrophic cardiomyocytes switch their metabolism from fatty acid oxidation to glucose use, but the functional role of this change is unclear. Here the authors show that high intracellular glucose inhibits the degradation of branched-chain amino acids, which is required for the activation of pro-growth mTOR signaling.

    • Dan Shao
    • , Outi Villet
    •  & Rong Tian

  • Article
    | Open Access

    AMPK activation inhibits cardiac hypertrophy. Here the authors show that this occurs independently of previously proposed mechanisms and that AMPK controls the phosphorylation of the aminotransferase GFAT, thereby preventing cardiac hypertrophy through the reduction of protein O-GlcNAcylation.

    • Roselle Gélinas
    • , Florence Mailleux
    •  & Luc Bertrand

  • Article
    | Open Access

    Transcriptome data provide only a partial picture of disease states. Here, via integration of transcript-, protein abundance and protein turnover data for a mouse model of cardiac hypertrophy, the authors uncover additional disease gene signatures, and show that turnover data sheds unique light on posttranslational regulation.

    • Edward Lau
    • , Quan Cao
    •  & Peipei Ping

  • Article
    | Open Access

    Little is known about the changes in mRNA splicing, processing and stability that can alter gene expression during heart failure. Here, the authors show that BEX1 is induced during heart failure and is part of a ribonucleoprotein complex enhancing the expression and stability of proinflammatory genes.

    • Federica Accornero
    • , Tobias G. Schips
    •  & Jeffery D. Molkentin

  • Article
    | Open Access

    Understanding the mechanisms causing cardiac fibrosis is key to prevention and therapy development of many heart diseases. Here, the authors show that Wnt/β-catenin signaling in resident cardiac fibroblasts is required for deposition of fibrotic extracellular matrix and the regulation of cardiomyocyte hypertrophy in a mouse model of heart fibrosis.

    • Fu-Li Xiang
    • , Ming Fang
    •  & Katherine E. Yutzey

  • Article
    | Open Access

    The human congenital disorder Noonan Syndrome (NS) is caused by germ-line mutations that hyperactivate the RAS/ERK signalling pathway, and can feature pathologic cardiac enlargement. Here, the authors find that a complex cellular and molecular interplay involving a cytokine hierarchy underlies cardiac hypertrophy caused by a NS-associatedRafallele.

    • Jiani C. Yin
    • , Mathew J. Platt
    •  & Benjamin G. Neel

  • Article
    | Open Access

    Abatacept is an FDA-approved drug used for treatment of rheumatoid arthritis. Here the authors show that abatacept reduces cardiomyocyte death in a mouse model of heart failure by inhibiting activation and heart infiltration of T cells and macrophages, an effect mediated by IL-10, suggesting a potential therapy for heart failure.

    • Marinos Kallikourdis
    • , Elisa Martini
    •  & Gianluigi Condorelli

  • Article
    | Open Access

    5-hydroxymethylation of cysteine (5-hmC) plays a role in epigenetic regulation. Here the authors analyse the hydroxymethylome in embryonic, neonatal, adult and hypertrophic mouse cardiomyocytes and show that the dynamic modulation of hydroxymethylated DNA is important for cardiomyocyte gene expression programming in heart development and failure.

    • Carolina M. Greco
    • , Paolo Kunderfranco
    •  & Gianluigi Condorelli

  • Article
    | Open Access

    Identifying pathways that cause pathological cardiac hypertrophy holds great therapeutic potential. Here the authors discover one such pathway and show that SIKE, an inhibitor of interferon signalling, prevents pathological but not physiological cardiac hypertrophy by interacting with TBK1 and modulating the TBK1/AKT signalling in rodents and monkeys.

    • Ke-Qiong Deng
    • , Aibing Wang
    •  & Hongliang Li

  • Article
    | Open Access

    Restricting hypertrophic heart growth in response to pathologic overload is an unmet therapeutic need. Here, the authors show that blocking Ca2+signaling controlled by the transport protein PMCA4 in cardiac fibroblasts enhances secretion of a potent Wnt signaling inhibitor, sFRP2, and prevents the development of pathologic cardiac hypertrophy in mice.

    • Tamer M. A. Mohamed
    • , Riham Abou-Leisa
    •  & Delvac Oceandy

  • Article
    | Open Access

    mTOR signalling pathway is a critical regulator of cardiac hypertrophy. Here the authors show that two kinases, p38γ and p38δ, control heart growth by promoting mTOR activity via phosphorylation and consequent proteasome degradation of mTOR inhibitor DEPTOR, extending our knowledge of cardiac hypertrophy regulation.

    • Bárbara González-Terán
    • , Juan Antonio López
    •  & Guadalupe Sabio

  • Article |

    The chemical honokiol is found in the bark of magnolia trees, which are used for traditional medicine in Asian countries. Here, Pillai et al, show honokiol protects the heart from hypertrophic remodelling in mice, and even reverses established cardiac hypertrophy, by activating the deacetylase Sirt3.

    • Vinodkumar B. Pillai
    • , Sadhana Samant
    •  & Mahesh P. Gupta

  • Article
    | Open Access

    The transcription factor interferon regulatory factor 8 (IRF8) is known to regulate differentiation and function of immune cells. Here the authors show that IRF8 is upregulated in the hypertrophic heart in humans and mice, where it suppresses cardiac remodelling by inhibiting calcineurin signalling.

    • Ding-Sheng Jiang
    • , Xiang Wei
    •  & Hongliang Li

  • Article
    | Open Access

    Heart failure is often a consequence of pathological growth of cardiomyocytes or cardiac hypertrophy. Here Ucar and colleagues report that the microRNAs miR-132 and miR-212 promote cardiac hypertrophy and inhibit autophagy in cardiomyocytes by downregulating the transcription factor FoxO3.

    • Ahmet Ucar
    • , Shashi K. Gupta
    •  & Thomas Thum

  • Article
    | Open Access

    The tumour suppressor BRCA1 is mutated in familial breast and ovarian cancer. Now, Shuklaet al.demonstrate that mice lacking BRCA1 in cardiomyocytes are more sensitive to ischaemia than control mice, and that BRCA1 is elevated in human tissues exposed to ischaemia, suggesting a cardioprotective role for BRCA1.

    • Praphulla C. Shukla
    • , Krishna K. Singh
    •  & Subodh Verma

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