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Macrophage production of MT1-MMP upon MI contributes to adverse cardiac remodeling and worsened function by promoting EndMT via TGFB, suggesting MT1-MMP inhibition as a therapeutic option for patients with MI.

Maternal loss of imprinting at the Igf2/H19 locus reduces expression of H19 lncRNA and thereby leads to progressive cardiac pathologies in a mouse Beckwith–Wiedemann syndrome model.

Personalized virtual-heart technology for arrhythmia risk assessment could transform the management of hypertrophic cardiomyopathy patients, eliminating many unnecessary primary-prevention defibrillator deployments while ensuring patients at high risk for arrhythmia are adequately protected.

Reative oxygen species modulate microtubules and diaphragm function.

Inhibition of RyR2 hyperactivity with dantrolene not only prevents VT/VF and SCD but also heart failure by mitigating calcium dysfunction in pressure-overloaded hearts.

SARS-CoV-2 infection in hamsters causes cardiovascular pathologies.

Activation of TRPV4 induced increases in Ca²⁺ influx, activated CaMKII, enhanced pro-inflammatory NFκB-NLRP3 signaling, and promoted inflammation response, thus contributing to pathological cardiac remodeling.

Ex vivo, in vitro, and computational modeling studies indicate a persistence of myofibroblast senescence in the infarct border zone with age which can disrupt conduction and promote arrhythmias via senescent myofibroblast-cardiomyocyte coupling.

Lack of cardiac MKK6 results in premature death with the development of heart hypertrophy and cardiac dysfunction in aging.

FHOD1 and CARP/Ankrd1 interact with the N-terminal region of palladin and cardiomyocyte-specific deletion of palladin in adult, but not embryonic, mice leads to dilated cardiomyopathy associated with intercalated disc widening.