What is the clinical evidence from this study?

Population: Cardiac hypertrophy. Intervention: Cardiac-specific overexpression of DGKzeta vs. Wild-type littermate mice. Primary outcome: GPCR agonist-induced cardiac hypertrophy (cross-sectional cardiomyocyte areas and heart to body weight ratios).

December 28, 2005Circulation

Cardiac-Specific Overexpression of Diacylglycerol Kinase ζ Prevents Gq Protein-Coupled Receptor Agonist-Induced Cardiac Hypertrophy in Transgenic Mice

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Key result

Cardiac-specific overexpression of DGKzeta in transgenic mice completely blocked GPCR agonist-induced PKC translocation, ANF upregulation, and subsequent cardiac hypertrophy compared to wild-type mice.

Why the study?

Does cardiac-specific overexpression of DGKzeta prevent GPCR agonist-induced cardiac hypertrophy in mice?

Population

Transgenic mice with cardiac-specific overexpression of diacylglycerol kinase zeta and wild-type littermate…

Comparison

Continuous administration of subpressor doses of… vs Wild-type littermate mice receiving the same…

Design

Preclinical

Authors

TATakanori ArimotoYamagata University YTYasuchika TakeishiHeart Failure & Transplant HTHiroki TakahashiSapporo Medical University

Discussion

Member takes

Implication

Hypothesis-generating for DGKzeta modulation in hypertrophy; leaves open translation to human disease or therapy.

Structured PICO

Does cardiac-specific overexpression of DGKzeta prevent GPCR agonist-induced cardiac hypertrophy in mice?

Population

Transgenic mice with cardiac-specific overexpression of DGKzeta and wild-type littermates subjected to continuous administration of subpressor doses of angiotensin II and phenylephrine.

Intervention

Continuous administration of subpressor doses of angiotensin II and phenylephrine

Comparator

Wild-type littermate mice receiving the same GPCR agonists

Outcome

Cardiac hypertrophy (measured by cross-sectional cardiomyocyte areas and heart to body weight ratios) and hypertrophic signaling (PKC translocation, atrial natriuretic factor gene expression)surrogate

Cardiac-specific overexpression of DGKzeta prevents GPCR agonist-induced cardiac hypertrophy in transgenic mice by regulating cellular diacylglycerol levels and PKC activity.

Cite This Study

Arimoto et al. (2005) studied Cardiac hypertrophy. Cardiac-specific overexpression of DGKzeta vs. Wild-type littermate mice was evaluated on GPCR agonist-induced cardiac hypertrophy (cross-sectional cardiomyocyte areas and heart to body weight ratios). Cardiac-specific overexpression of DGKzeta in transgenic mice completely blocked GPCR agonist-induced PKC translocation, ANF upregulation, and subsequent cardiac hypertrophy compared to wild-type mice.

synapsesocial.com/papers/6a8fa3581403187eefcb4173 https://doi.org/10.1161/circulationaha.105.560771

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Cardiac-Specific Overexpression of Diacylglycerol Kinase ζ Prevents Gq Protein-Coupled Receptor Agonist-Induced Cardiac Hypertrophy in Transgenic Mice

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Cardiac-Specific Overexpression of Diacylglycerol Kinase ζ Prevents Gq Protein-Coupled Receptor Agonist-Induced Cardiac Hypertrophy in Transgenic Mice

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider