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Articles by William Pu
SORBS2 regulates diastolic function through cytoskeletal networks and calcium handling
Abstract Diastolic dysfunction, defined by impaired relaxation and increased ventricular stiffness, is central to heart failure with preserved ejection fraction, yet cardiomyocyte-intrinsic mechanisms remain incompletely understood. Here, we show that SORBS2 is a vital component of murine cardiomyocyte adhesion complexes. Its genetic ablation in mice causes progressive diastolic dysfunction with preserved systolic function, accompanied by atrial enlargement and reduced survival.
Nrf1 coordinates proteasome activity and autophagy to maintain cardiac proteostasis
Abstract Proteolytic stress frequently arises during disease and aging, particularly in long-lived, post-mitotic cells such as cardiomyocytes. To maintain proteostasis, cardiomyocytes depend on coordinated protein quality control pathways, including the ubiquitin-proteasome system and autophagy. Mechanisms that activate these pathways hold therapeutic potential for heart disease.
TBX5 and CHD4 Coordinately Activate Atrial Cardiomyocyte Genes to Maintain Cardiac Rhythm Homeostasis
Clinical Perspective • TBX5 (T-box 5), a transcription factor implicated in human atrial fibrillation (AF) by genome-wide association studies, regulates atrial cardiomyocyte gene transcription by recruiting a chromatin remodeling enzyme, CHD4 (chromodomain helicase DNA binding protein 4), to control the accessibility of cis-regulatory elements.
Dysregulation of N-terminal acetylation causes cardiac arrhythmia and cardiomyopathy - Nature Communications
Abstract N-terminal acetyltransferases including NAA10 catalyze N-terminal acetylation, an evolutionarily conserved co- and post-translational modification. However, little is known about the role of N-terminal acetylation in cardiac homeostasis. To gain insight into cardiac-dependent NAA10 function, we studied a previously unidentified NAA10 variant p.(Arg4Ser) segregating with QT-prolongation, cardiomyopathy, and developmental delay in a large kindred.
Fibre-infused gel scaffolds guide cardiomyocyte alignment in 3D-printed ventricles - Nature Materials
Abstract Hydrogels are attractive materials for tissue engineering, but efforts to date have shown limited ability to produce the microstructural features necessary to promote cellular self-organization into hierarchical three-dimensional (3D) organ models. Here we develop a hydrogel ink containing prefabricated gelatin fibres to print 3D organ-level scaffolds that recapitulate the intra- and intercellular organization of the heart.
Molecule in mothers’ milk nurses pups’ heart cells to maturity
Guo, Y. & Pu, W. T. Circ. Res. 126, 1086–1106 (2020). Article PubMed Google Scholar Paredes, A. et al. Nature https://doi.org/10.1038/s41586-023-06068-7 (2023). Article Google Scholar Shao, M. et al. Biomed. Pharmacother. 137, 111264 (2021). Article PubMed Google Scholar Heyman, R. A. et al. Cell 68, 397–406 (1992). Article PubMed Google Scholar Sergeant, S., Rahbar, E. & Chilton, F. H. Eur. J. Pharmacol. 785, 77–86 (2016). Article PubMed Google Scholar Vega, R. B, Huss, J. M. & Kelly, D. P. Mol. Cell Biol.
Depletion of VGLL4 Causes Perinatal Lethality without Affecting Myocardial Development
Open AccessArticle by Caroline Sheldon 1, Aaron Farley 1,2, Qing Ma 3, William T. Pu 3 and Zhiqiang Lin 1,* 1 Masonic Medical Research Institute, 2150 Bleecker St., Utica, NY 13501, USA 2 Biology and Chemistry Department, SUNY Polytechnic Institute, 100 Seymour Rd., Utica, NY 13502, USA 3 Department of Cardiology, Boston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02115, USA * Author to whom correspondence should be addressed.
Calcific aortic valve disease: turning therapeutic discovery up a notch
Valve replacement is currently the only treatment for calcific aortic valve disease. Studies of an uncommon, genetic form of aortic valve disease have yielded in vitro and mouse models of the disease and a transcriptomic disease signature. Machine learning-driven screens for compounds that normalize this signature promise to enable medical management of aortic valve disease. Refers to Theodoris, C. V. et al.
Genetic Mosaics for Greater Precision in Cardiovascular Research
Defining cell-autonomous effects using genetic mosaics. A, Comparison of whole-organ vs mosaic gene manipulation. Gene in knocked out in most cardiomyocytes often results in organ dysfunction, leading to cell nonautonomous effects that amplify and obscure the direct effect. In the mosaic knockout, the unaffected cardiomyocytes limit the nonautonomous effects and thereby allow the investigator to identify the cell-autonomous effects.
Exercising engineered heart muscle to maturity
The immaturity of stem cell-derived cardiomyocytes has impeded their use for in vitro disease modelling, cardiotoxicity assays, and cell-replacement therapy. Ronaldson-Bouchard and colleagues report unparalleled in vitro maturation of stem cell-derived cardiomyocytes. This advance promises to unlock the translational potential of these cells.
Molecule in mothers' milk nurses pups' heart cells to maturity
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