Results 141 to 150 of about 607,470 (403)

Patient and Disease-Specific Induced Pluripotent Stem Cells for Discovery of Personalized Cardiovascular Drugs and Therapeutics. [PDF]

open access: yes, 2020
Human induced pluripotent stem cells (iPSCs) have emerged as an effective platform for regenerative therapy, disease modeling, and drug discovery.
Chandy, Mark   +2 more
core  

ALKBH5‐Mediated M6A Demethylation of G3BP1 Attenuates Ferroptosis Via Cytoplasmic Retention of YBX1/p53 in Diabetic Myocardial Ischemia‐Reperfusion Injury

open access: yesAdvanced Science, EarlyView.
ALKBH5 promoted G3BP1 expression via m⁶A methylation at sites 142/173. G3BP1 interacts with YBX1 and p53, reducing their nuclear translocation and decreasing p53‐mediated SLC7A11 repression. This inhibites cardiomyocyte ferroptosis and mitigates myocardial damage during diabetic ischemia‐reperfusion injury.
Wenyuan Li   +5 more
wiley   +1 more source

Genetically engineered biomimetic ATP-responsive nanozyme for the treatment of cardiac fibrosis

open access: yesJournal of Nanobiotechnology
Background Cardiac fibrosis plays a critical role in the progression of various forms of heart disease, significantly increasing the risk of sudden cardiac death.
Xueli Zhao   +13 more
doaj   +1 more source

Cardiomyopathy in Children: Classification and Diagnosis: A Scientific Statement From the American Heart Association.

open access: yesCirculation, 2019
In this scientific statement from the American Heart Association, experts in the field of cardiomyopathy (heart muscle disease) in children address 2 issues: the most current understanding of the causes of cardiomyopathy in children and the optimal ...
S. Lipshultz   +10 more
semanticscholar   +1 more source

Is arrhythmogenic right ventricular cardiomyopathy a paediatric problem too? [PDF]

open access: yes, 2001
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a heart muscle disease that is often familial, characterized by arrhythmias of right ventricular origin, due to transmural fatty or fibrofatty replacement of atrophic myocardium. ARVC is usually
Basso, Cristina   +4 more
core  

Arrhythmogenic right ventricular cardiomyopathy associated with severe left ventricular involvement in a cat. [PDF]

open access: yes, 2009
An 8-year-old, 4 kg, intact female, domestic shorthaired cat was referred for tachypnea and pleural effusion. A 24-h Holter recording showed numerous polymorphic ventricular premature complexes with left and right bundle branch block morphology ...
Basso C   +3 more
core   +1 more source

LncRNA Foxo6os as a Novel “ Scaffold” Mediates MYBPC3 in Combating Pathological Cardiac Hypertrophy and Heart Failure

open access: yesAdvanced Science, EarlyView.
Schematic overview showing that forkhead box O6, opposite strand (Foxo6os) acts as a “scaffold”, directly binding myosin‐binding protein‐C (MYBPC3) and recruiting protein kinase C (PKC‐α) to mediate site‐specific phosphorylation of MYBPC3. This post‐translational modification supports cardiac contraction by regulating L‐type Ca2+ channels, especially ...
Jie Sheng   +9 more
wiley   +1 more source

Weight loss in hypertrophic cardiomyopathy: A clinical case series

open access: yesInternational Journal of Cardiology. Cardiovascular Risk and Prevention, 2023
Background: Obesity is prevalent among patients with hypertrophic cardiomyopathy (HCM). Obese HCM patients have greater wall thickness, LV mass, worse hemodynamic function and NYHA class. Weight loss may favorably influence the HCM phenotype.
Maria C. Reuter   +6 more
doaj  

Feline Hypertrophic Cardiomyopathy: A Spontaneous Large Animal Model of Human HCM. [PDF]

open access: yes, 2017
Hypertrophic cardiomyopathy (HCM) is a common disease in pet cats, affecting 10-15% of the pet cat population. The similarity to human HCM, the rapid progression of disease, and the defined and readily determined endpoints of feline HCM make it an ...
Freeman, Lisa M   +4 more
core   +2 more sources

Atrial Fibroblasts‐Derived Extracellular Vesicles Exacerbate Atrial Arrhythmogenesis

open access: yesAdvanced Science, EarlyView.
Exosome miR‐224‐5p derived from angiotensin II‐treated atrial fibroblasts creates a substrate for AF by promoting atrial electrical remodeling. Increased exosome miR‐224‐5p enhances AF susceptibility by inhibiting CACNA1c expression and decreasing ICa current of atrial cardiomyocytes.
Yue Yuan   +13 more
wiley   +1 more source

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