February 13, 2018The FASEB Journal
Immune responsive resolvin D1 programs myocardial infarction‐induced cardiorenal syndrome in heart failure
Key result
Exogenous resolvin D1 cleared MI-induced inflammation by increasing resolving leukocytes and facilitated renoprotective mechanisms to limit cardiorenal syndrome in mice.
Why the study?
Does resolvin D1 reduce cardiorenal inflammation and remodeling in a mouse model of myocardial infarction?
Population
8- to 12-wk-old male C57BL/6 mice subjected to coronary artery ligation (myocardial infarction model)
Comparison
Resolvin D1 injected 3 hours after myocardial… vs Myocardial infarction mice with no treatment and…
Design
Preclinical
Follow-up
up to 28 days
Authors
Discussion
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Implication
RvD1 attenuates post-MI cardiorenal inflammation in mice; leaves open whether exogenous resolvins limit CRS in patients.
Structured PICO
Does resolvin D1 reduce cardiorenal inflammation and remodeling in a mouse model of myocardial infarction?
P
Population
8- to 12-week-old male C57BL/6 mice subjected to coronary artery ligation to study post-MI cardiorenal syndrome.
I
Intervention
Resolvin D1 (RvD1) injected 3 hours after myocardial infarction
C
Comparator
Myocardial infarction mice with no treatment (MI controls) and mice with no surgery (naive controls)
O
Outcome
Cardiorenal inflammation and remodeling (neutrophil clearance, reparative macrophages, miRNA storm, nephrin expression, renal inflammation)surrogate
In a mouse model of myocardial infarction, resolvin D1 clears inflammation and facilitates renoprotective mechanisms to limit cardiorenal syndrome.
Cite This Study
Halade et al. (2018) studied Myocardial infarction-induced cardiorenal syndrome. Resolvin D1 (RvD1) vs. MI controls with no treatment was evaluated on MI-induced cardiorenal inflammation and renal injury. Exogenous resolvin D1 cleared MI-induced inflammation by increasing resolving leukocytes and facilitated renoprotective mechanisms to limit cardiorenal syndrome in mice.