Key result
CD11b/CD18 integrin deficiency protected mice from angiotensin II-induced atrial fibrosis and significantly reduced the vulnerability to atrial fibrillation compared to wild-type mice.
Why the study?
Does CD11b/CD18 deficiency prevent angiotensin II-induced atrial fibrillation and fibrosis in mice?
Population
Male C57bl/6J wildtype and CD11b/CD18 knock-out mice, plus right atrial appendages from human patients with…
Comparison
Angiotensin II via subcutaneously implanted… vs Vehicle via subcutaneously implanted osmotic…
Design
Preclinical
Follow-up
14 days
Authors
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Hypothesis-generating for integrin blockade in experimental AF; leaves open any role in human disease.
Does CD11b/CD18 deficiency prevent angiotensin II-induced atrial fibrillation and fibrosis in mice?
p-value: p=<0.05
CD11b/CD18 integrin-mediated neutrophil infiltration is critical for the development of atrial fibrosis and the initiation and propagation of atrial fibrillation.
Friedrichs et al. (2014) studied Atrial Fibrillation. CD11b/CD18 deficiency vs. Wild-type was evaluated on Number and duration of AF episodes upon electrophysiological stimulation (p=<0.05). CD11b/CD18 integrin deficiency protected mice from angiotensin II-induced atrial fibrosis and significantly reduced the vulnerability to atrial fibrillation compared to wild-type mice.
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