about
Silencing of miR-34a attenuates cardiac dysfunction in a setting of moderate, but not severe, hypertrophic cardiomyopathy.Therapeutic inhibition of the miR-34 family attenuates pathological cardiac remodeling and improves heart functionInhibition of miR-154 Protects Against Cardiac Dysfunction and Fibrosis in a Mouse Model of Pressure OverloadPathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets.Phosphoinositide 3-kinase p110α is a master regulator of exercise-induced cardioprotection and PI3K gene therapy rescues cardiac dysfunction.Distinct lipidomic profiles in models of physiological and pathological cardiac remodeling, and potential therapeutic strategies.Gene delivery of medium chain acyl-coenzyme A dehydrogenase (MCAD) induces physiological cardiac hypertrophy and protects against pathological remodelling.Sex differences in response to miRNA-34a therapy in mouse models of cardiac disease: identification of sex-, disease- and treatment-regulated miRNAs.Enhanced phosphoinositide 3-kinase(p110α) activity prevents diabetes-induced cardiomyopathy and superoxide generation in a mouse model of diabetes.The small-molecule BGP-15 protects against heart failure and atrial fibrillation in mice.Therapeutic silencing of miR-652 restores heart function and attenuates adverse remodeling in a setting of established pathological hypertrophy
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description
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Yow Keat Tham
@ast
Yow Keat Tham
@en
Yow Keat Tham
@es
Yow Keat Tham
@nl
type
label
Yow Keat Tham
@ast
Yow Keat Tham
@en
Yow Keat Tham
@es
Yow Keat Tham
@nl
prefLabel
Yow Keat Tham
@ast
Yow Keat Tham
@en
Yow Keat Tham
@es
Yow Keat Tham
@nl
P106
P1153
55328324100
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P496
0000-0002-9790-1926