October 1, 2019European Heart Journal

P5000Wnt/b-catenin signalling drives angiotensin II induced cardiac fibrosis via WISP-1

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Why the study?

The mechanisms driving pathological collagen deposition are not fully elucidated, and the role of Wnt signaling and its product WISP-1 in cardiac fibrosis remains debated.

Population

Human cardiac fibroblasts in vitro and Apolipoprotein E−/−/WISP-1+/+ vs ApolipoproteinE−/−/WISP-1−/− mice (n=6–8)

Comparison

AngII infusion vs control, and WISP-1+/+ vs WISP-1−/−

Design

In vitro and in vivo preclinical animal study

Follow-up

4 weeks

Authors

GCGeorgia May ConnollyNIHR Bristol Cardiovascular Biomedical Research Unit ZLZ LiUniversity of Bristol MYMark T. YoungCardiff University

Discussion

Member takes

Implication

Supports WISP-1 as mediator of AngII fibrosis in models; leaves open clinical translation.

Structured PICO

Population

In vitro human cardiac fibroblasts and in vivo Apolipoprotein E−/−/WISP-1+/+ vs. ApolipoproteinE−/−/WISP-1−/− mice on a high-fat diet (n=6-8)

Intervention

Angiotensin II (100nM in vitro, 500ng/kg/min in vivo for 4 weeks) and Wnt/b-catenin inhibitor iCRT14 (25nM in vitro)

Comparator

Control (no AngII) and WISP-1+/+ mice

Outcome

Collagen type 1 protein levelssurrogate

Angiotensin II drives cardiac fibrosis via the Wnt/β-catenin signalling pathway and WISP-1, highlighting a potential therapeutic target for preventing myocardial stiffening.

Cite This Study

Connolly et al. (2019) studied this question.

synapsesocial.com/papers/69d81bfa617ce96c42ae2fe6 https://doi.org/10.1093/eurheartj/ehz746.0178

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