June 7, 2005CirculationOpen Access

Calcineurin–Nuclear Factor of Activated T Cells Pathway–Dependent Cardiac Remodeling in Mice Deficient in Guanylyl Cyclase A, a Receptor for Atrial and Brain Natriuretic Peptides

View Full Paper

Ask AI

Bookmark

Structured PICO

Population

Guanylyl cyclase A-knockout (GCA-KO) mice, wild-type (WT) mice, and neonatal cultured cardiac myocytes

Intervention

FK506 (6 mg/kg body weight subcutaneously once daily from 10 to 14 weeks of age) in mice; HS142-1 (100 microg/mL) or atrial natriuretic peptide (10^-6 mol/L) in cultured myocytes

Comparator

Untreated GCA-KO mice, WT mice, and untreated cultured myocytes

Outcome

Cardiac remodeling parameters including heart-to-body weight ratio, cardiomyocyte size, collagen volume fraction, and calcineurin-NFAT pathway activitysurrogate

The study demonstrates that natriuretic peptides protect the heart from excessive remodeling by inhibiting the calcineurin-NFAT pathway via guanylyl cyclase A.

Discussion

No takes yet. Share an insight, caveat, or question.

Implication

Calcineurin-NFAT inhibition attenuates remodeling downstream of GC-A; hypothesis-generating in mice and leaves open human translation.

Cite This Study

Tokudome et al. (2005) studied this question.

synapsesocial.com/papers/6a7564001646b2abe5036b93 https://doi.org/10.1161/circulationaha.104.510594

View Full Paper

Ask AI

Bookmark

Calcineurin–Nuclear Factor of Activated T Cells Pathway–Dependent Cardiac Remodeling in Mice Deficient in Guanylyl Cyclase A, a Receptor for Atrial and Brain Natriuretic Peptides

Structured PICO

Discussion

Implication

Cite This Study

Calcineurin–Nuclear Factor of Activated T Cells Pathway–Dependent Cardiac Remodeling in Mice Deficient in Guanylyl Cyclase A, a Receptor for Atrial and Brain Natriuretic Peptides

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider