Key result
Human recombinant AnxA1 halts and reverses diastolic dysfunction in an inflammatory arthritis mouse model.
Why the study?
The causes of diastolic dysfunction in rheumatoid arthritis are unknown, well-characterized animal models are lacking, and current medications do not provide marked cardioprotective effects.
Does human recombinant AnxA1 improve cardiac diastolic dysfunction in mice with inflammatory arthritis?
Population
K/BxN F1 progeny and KRN control mice
Comparison
Human recombinant AnxA1 (hrAnxA1, 1 microg/mouse) vs vehicle daily
Design
Animal and pharmacological experimental study
Authors
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AnxA1 merits further preclinical testing in HFpEF; leaves open translation to human inflammatory arthritis.
Does human recombinant AnxA1 improve cardiac diastolic dysfunction in mice with inflammatory arthritis?
In a mouse model of inflammatory arthritis, treatment with human recombinant Annexin A1 corrected diastolic dysfunction by modulating fibroblast and inflammatory cell phenotypes.
Chen et al. (2021) studied Inflammatory arthritis with cardiac diastolic dysfunction. human recombinant AnxA1 (hrAnxA1) vs. vehicle was evaluated on left ventricular diastolic and systolic function. Daily treatment with human recombinant AnxA1 (1 μg/mouse) halted the progression of diastolic dysfunction and corrected it after disease onset in a mouse model of inflammatory arthritis.
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