November 19, 2014Cardiovascular ResearchOpen Access

Exchange protein directly activated by cAMP 1 promotes autophagy during cardiomyocyte hypertrophy

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Population

Neonatal cardiomyocytes and Epac1 knockout mice

Comparison

Epac1 stimulation, β-AR stimulation, Epac1… vs Control cardiomyocytes and wild-type mice

Design

Preclinical

Authors

ALAnne‐Coline LaurentGuerbet (France)MBMalik BisserierNew York Medical College ALAlexandre LucasUniversité Paris-Sud

Discussion

Member takes

Implication

Hypothesis-generating for Epac1-autophagy targeting in HF; leaves open translation to human disease and trials.

Structured PICO

Population

Neonatal cardiomyocytes and Epac1 knockout mice

Intervention

Epac1 stimulation (Sp-8-pCPT), β-AR stimulation (isoprenaline), Epac1 inhibition (CE3F4), Epac1 deletion, and autophagy inhibition (3-MA or Atg5 down-regulation)

Comparator

Control cardiomyocytes and wild-type mice

Outcome

Autophagy activation and cardiomyocyte hypertrophy/cardiac remodellingsurrogate

Autophagy acts as an adaptive, protective response to antagonize Epac1-promoted cardiomyocyte hypertrophy.

Cite This Study

Laurent et al. (2014) studied this question.

synapsesocial.com/papers/6a780630576efb0ddaf7d46c https://doi.org/10.1093/cvr/cvu242

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Ask AI

Bookmark

Exchange protein directly activated by cAMP 1 promotes autophagy during cardiomyocyte hypertrophy

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Exchange protein directly activated by cAMP 1 promotes autophagy during cardiomyocyte hypertrophy

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider