Key result
Genetic ablation of the long non-coding RNA Malat-1 did not significantly affect cardiac hypertrophy or left ventricular fractional shortening in mice subjected to pressure overload.
Why the study?
Does Malat-1 deficiency affect cardiac hypertrophy and failure during pressure overload in mice?
Does Malat-1 deficiency affect cardiac hypertrophy and failure during pressure overload in mice?
Absolute Event Rate: 8.91% vs 9.79%
The long non-coding RNA Malat-1 is dispensable for pressure overload-induced cardiac remodeling and failure in mice, suggesting it does not play a critical role in this pathology despite its known functions in mRNA splicing.
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Malat-1 ablation shows no remodeling effect in murine pressure overload; leaves open its relevance to human heart failure and need for validation in other models.
Peters et al. (2016) studied Pressure overload-induced cardiac remodeling and failure. Malat-1 knockout vs. Malat-1 wild-type was evaluated on Heart weight to tibia length ratio (g/mm) after thoracic aortic constriction. Genetic ablation of the long non-coding RNA Malat-1 did not significantly affect cardiac hypertrophy or left ventricular fractional shortening in mice subjected to pressure overload.
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