S ‐Nitrosoglutathione Reductase Deficiency Enhances the Proliferative Expansion of Adult Heart Progenitors and Myocytes Post Myocardial Infarction
Why the study?
Does GSNOR deficiency improve cardiac regenerative activity and function post-MI in a mouse model?
Population
112 mice: GSNOR and C57Bl6/J mice subjected to sham operation (n=3 GSNOR; n=3 WT) or myocardial infarction…
Comparison
GSNOR deficiency (GSNOR(-/-) genetic knockout) vs Wild-type (WT) C57Bl6/J mice
Design
Preclinical
Authors
Discussion
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Member takes
Implication
GSNOR deficiency may enhance post-MI regeneration in mice; leaves open translation to human cardiac repair.
Structured PICO
Does GSNOR deficiency improve cardiac regenerative activity and function post-MI in a mouse model?
P
Population
112 mice: GSNOR(-/-) and C57Bl6/J (wild-type [WT]) mice subjected to sham operation (n=3 GSNOR(-/-); n=3 WT) or myocardial infarction (n=41 GSNOR(-/-); n=65 WT).
I
Intervention
GSNOR deficiency (GSNOR(-/-) genetic knockout)
C
Comparator
Wild-type (WT) C57Bl6/J mice
O
Outcome
Survival, cardiac performance (ejection fraction, endocardial volumes), scar size, and cellular proliferation post-MIsurrogate
GSNOR deficiency enhances post-MI cardiac regenerative activity and improves cardiac function, suggesting endogenous denitrosylases as a potential therapeutic target for cardiac repair.
Cite This Study
Hatzistergos et al. (2015) studied this question.