Key result
miR-133a is a promising therapeutic target for heart failure due to its role as a master regulator of networks controlling pathological cardiac remodeling.
Why the study?
Does overexpression of miR-133a ameliorate left ventricular function in failing hearts?
Does overexpression of miR-133a ameliorate left ventricular function in failing hearts?
miR-133a is highlighted as a promising therapeutic target for heart failure due to its multidisciplinary role in mitigating cardiac hypertrophy, fibrosis, and apoptosis.
Does not yet warrant clinical use of miR-133a therapies; leaves open whether overexpression improves LV function in randomized trials.
Although miR-133 mitigates cardiac hypertrophy and fibrosis, fine tunes β1-AR signaling, and protects against oxidative stress mediated apoptosis, it is unclear whether overexpression of miR-133a can ameliorate left ventricular function in failing hearts. Considering its multidisciplinary role in the heart, it is suggested that miR-133a is a master regulator of several networks that controls pathological cardiac remodeling. Therefore, it is a promising therapeutic target for heart failure.
No takes yet. Share an insight, caveat, or question.
Paras K. Mishra (2014) conducted a review in Heart failure. miR-133a was evaluated. miR-133a is a promising therapeutic target for heart failure due to its role as a master regulator of networks controlling pathological cardiac remodeling.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: