Results 71 to 80 of about 26,699 (253)

Fhod3 in zebrafish supports myofibril stability during growth of embryonic skeletal muscle

Developmental Dynamics, EarlyView.
Abstract Background Actin filament organization in cardiomyocytes critically depends on the formin Fhod3, but a role for Fhod3 in skeletal muscle development has not yet been described. Results We demonstrate here that in zebrafish mutated for one of two fhod3 paralog genes, fhod3a, skeletal muscle of the trunk appears normal through 2 days post ...
Aubrie Russell, Tracy Eng, Jeffrey D. Amack, David Pruyne   +3 more
wiley   +1 more source

Hypertrophic Cardiomyopathy with Special Focus on Mavacamten and Its Future in Cardiology

Biomedicines
Hypertrophic cardiomyopathy (HCM) is a heterogeneous group of heart muscle disorders that affects millions, with an incidence from 1 in 500 to 1 in 200. Factors such as genetics, age, gender, comorbidities, and environmental factors may contribute to the
Ewelina Młynarska, Ewa Radzioch, Bartłomiej Dąbek, Klaudia Leszto, Alicja Witkowska, Witold Czarnik, Weronika Jędraszak, Jacek Rysz, Beata Franczyk   +8 more
doaj   +1 more source

A transgenic platform for testing drugs intended for reversal of cardiac remodeling identifies a novel 11βHSD1 inhibitor rescuing hypertrophy independently of re-vascularization.

PLoS ONE, 2014
RationaleRescuing adverse myocardial remodeling is an unmet clinical goal and, correspondingly, pharmacological means for its intended reversal are urgently needed.ObjectivesTo harness a newly-developed experimental model recapitulating progressive heart
Oren Gordon, Zhiheng He, Dan Gilon, Sabine Gruener, Sherrie Pietranico-Cole, Amit Oppenheim, Eli Keshet   +6 more
doaj   +1 more source

The clinical characteristics of families with hypertrophic cardiomyopathy associated with mutations of cardiac myosin binding protein C

, 2010
Introduction: Mutations in cardiac myosin binding protein-C (MYBPC3), the most common genetic cause of hypertrophic cardiomyopathy (HCM), have been reported to cause a comparatively benign and late-onset form of the disease with incomplete penetrance ...
Page, S.P.
core  

Hypertrophic cardiomyopathy mutations in MYBPC3 dysregulate myosin

, 2019
The mechanisms by which truncating mutations in MYBPC3 (encoding cardiac myosin-binding protein C; cMyBPC) or myosin missense mutations cause hypercontractility and poor relaxation in hypertrophic cardiomyopathy (HCM) are incompletely understood.
Watkins, HC, Wakimoto, H, Lun, M, Lunde, IG, Seidman, JG, Watkins, Hugh, Toepfer, Christopher N., Gorham, JM, Jiang, J, McNamara, JW, Liao, D, Seidman, CE, Redwood, CS, Lynch, TL, Toepfer, CN, Garfinkel, AC, Redwood, Charles S., Sadayappan, S, McDonough, B, Tai, AC   +19 more
core   +1 more source

An ALPK3 truncation variant causing autosomal dominant hypertrophic cardiomyopathy is partially rescued by mavacamten

Scientific Reports
The ALPK3 gene encodes alpha-protein kinase 3, a cardiac pseudo-kinase of unknown function. Heterozygous truncating variants (ALPK3tv) can cause dominant adult-onset hypertrophic cardiomyopathy (HCM).
Lisa Leinhos, Paul Robinson, Giulia Poloni, Sophie Broadway-Stringer, Julia Beglov, Adam B. Lokman, Gillian Douglas, Sajjad Nuthay, Oveena Fonseka, Manuel Schmid, Evie Singer, Charlotte Hooper, Kate Thomson, Richard D. Bagnall, Jodie Ingles, Christopher Semsarian, Elizabeth Ormondroyd, Christopher N. Toepfer, Benjamin Davies, Charles Redwood, Hugh Watkins, Katja Gehmlich   +21 more
doaj   +1 more source

Gut microbiota‐related modulation of immune mechanisms in post‐infarction remodelling and heart failure

ESC Heart Failure, Volume 12, Issue 2, Page 942-954, April 2025.
Abstract The immune system has long been recognized as a key driver in the progression of heart failure (HF). However, clinical trials targeting immune effectors have consistently failed to improve patient outcome across different HF aetiologies. The activation of the immune system in HF is complex, involving a broad network of pro‐inflammatory and ...
Johann Roessler, Friederike Zimmermann, Bettina Heidecker, Ulf Landmesser, Arash Haghikia   +4 more
wiley   +1 more source

Proteasome inhibition slightly improves cardiac function in mice with hypertrophic cardiomyopathy

Frontiers in Physiology, 2014
A growing line of evidence indicates dysfunctional ubiquitin-proteasome system (UPS) in cardiac diseases. Anti-hypertrophic effects and improved cardiac function have been reported after treatment with proteasome inhibitors in experimental models of ...
Saskia eSchlossarek, Saskia eSchlossarek, Sonia eSingh, Sonia eSingh, Birgit eGeertz, Birgit eGeertz, Herbert eSchulz, Herbert eSchulz, Silke eReischmann, Silke eReischmann, Norbert eHübner, Norbert eHübner, Lucie eCarrier, Lucie eCarrier   +13 more
doaj   +1 more source

Cardiac remodelling in the era of the recommended four pillars heart failure medical therapy

ESC Heart Failure, Volume 12, Issue 2, Page 1029-1044, April 2025.
Abstract Cardiac remodelling is a key determinant of worse cardiovascular outcome in patients with heart failure (HF) and reduced ejection fraction (HFrEF). It affects both the left ventricle (LV) structure and function as well as the left atrium (LA) and the right ventricle (RV).
Giada Colombo, Tor Biering‐Sorensen, Joao P. Ferreira, Carlo Mario Lombardi, Andrea Bonelli, Andrea Garascia, Marco Metra, Riccardo M. Inciardi   +7 more
wiley   +1 more source

Mavacamten in Symptomatic Patients Resistant to Previous Advanced Therapy for Obstructive Hypertrophic Cardiomyopathy

Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Background The clinical benefits of mavacamten in patients with obstructive hypertrophic cardiomyopathy previously treated with advanced therapies are not established.
Daniele Massera, Elizabeth Adlestein, Sumar Frejat, Woon Y. Wu, Maria C. Reuter, Yuhe Xia, Isabel C. Alvarez, Mark V. Sherrid   +7 more
doaj   +1 more source