June 24, 2003Physiological Genomics

Deficiency of different nitric oxide synthase isoforms activates divergent transcriptional programs in cardiac hypertrophy

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Population

NOS-/- mice (NOS3-/- and NOS1-/-) and wild type (WT) mice

Comparison

Deletion of specific NOS isoforms (NOS3 or NOS1) vs Wild type (WT) mice

Design

Preclinical

Authors

TCThomas P. CappolaHeart Failure & Transplant LCLeslie CopeUniversity of North Carolina at Chapel Hill ACAmy CernetichJohns Hopkins University

Discussion

Member takes

Implication

Highlights isoform-specific cardiac gene regulation in NOS knockouts; leaves open human translation and therapeutic targeting.

Structured PICO

Population

NOS-/- mice (NOS3-/- and NOS1-/-) and wild type (WT) mice

Intervention

Deletion of specific NOS isoforms (NOS3 or NOS1)

Comparator

Wild type (WT) mice

Outcome

Cardiac gene expression profiles (Affymetrix MG-U74A)surrogate

Different NOS isoforms play distinct roles in modulating cardiac structure, as their deletion activates divergent transcriptional programs despite similar hypertrophic phenotypes.

Cite This Study

Cappola et al. (2003) studied this question.

synapsesocial.com/papers/6a7e293e884bedf30483dfba https://doi.org/10.1152/physiolgenomics.00156.2002

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Deficiency of different nitric oxide synthase isoforms activates divergent transcriptional programs in cardiac hypertrophy

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Deficiency of different nitric oxide synthase isoforms activates divergent transcriptional programs in cardiac hypertrophy

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider