Why the study?
The mechanisms of cardiac fibrosis in heart failure remain incompletely understood, prompting investigation into the molecular role of IGF1R in Ang II-induced cardiac fibrosis.
Does IGF1R deficiency alleviate Angiotensin II-induced cardiac fibrosis in mouse models?
Population
C57BL/6J and Igf1r+/- mice, primary mouse cardiac cells, and patients with heart failure
Comparison
IGF1R deficiency or inhibition vs controls under Ang II stimulation
Design
Preclinical in vitro and in vivo laboratory study with human observational blood samples
Follow-up
2 weeks
Key result
IGF1R signaling deficiency alleviated Angiotensin II-induced cardiac fibrosis in mice, partially through inhibiting endothelial-mesenchymal transition via the Akt/ERK/NF-κB pathway.
Authors
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Animal findings suggest IGF1R as fibrosis target; leaves open translation to human disease.
Does IGF1R deficiency alleviate Angiotensin II-induced cardiac fibrosis in mouse models?
IGF1R signaling deficiency alleviates Angiotensin II-induced cardiac fibrosis by inhibiting endothelial-mesenchymal transition via the Akt/ERK/NF-κB pathway, suggesting IGF1R as a potential therapeutic target.
Zhu et al. (2023) studied Cardiac fibrosis. IGF1R deficiency (Igf1r+/- mice) vs. Wild type mice was evaluated on Cardiac fibrosis and endothelial-mesenchymal transition. IGF1R signaling deficiency alleviated Angiotensin II-induced cardiac fibrosis in mice, partially through inhibiting endothelial-mesenchymal transition via the Akt/ERK/NF-κB pathway.
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