Reducing Endoglin Activity Limits Calcineurin and TRPC‐6 Expression and Improves Survival in a Mouse Model of Right Ventricular Pressure Overload
Why the study?
Does reducing endoglin activity improve survival and limit RV fibrosis in mouse models of right ventricular pressure overload?
Population
Human RV fibroblasts, endoglin haploinsufficient mice, and wild-type mice with right ventricular pressure…
Comparison
Reduced endoglin activity via genetic… vs Wild-type mice or immunoglobulin G (IgG) control
Design
Preclinical
Authors
Discussion
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Implication
Endoglin targeting may offer a novel RV failure strategy; leaves open translation from mouse models to clinical use.
Structured PICO
Does reducing endoglin activity improve survival and limit RV fibrosis in mouse models of right ventricular pressure overload?
P
Population
Human RV fibroblasts, endoglin haploinsufficient mice (Eng+/-), and wild-type mice with right ventricular pressure overload (RVPO) induced by pulmonary artery constriction or angio-obliterative pulmonary hypertension
I
Intervention
Reduced endoglin activity via genetic haploinsufficiency (Eng+/-) or neutralizing antibody against endoglin (N-Eng)
C
Comparator
Wild-type mice or immunoglobulin G (IgG) control
O
Outcome
Survival, RV function, RV fibrosis, and calcineurin/TRPC-6/α-SMA pathway activationsurrogate
Targeting endoglin to reduce its activity limits RV fibrosis and improves survival in preclinical models of right ventricular pressure overload, suggesting a potential therapeutic target for RV failure.
Cite This Study
Kapur et al. (2014) studied this question.