Why the study?
It was unknown whether the diabetic milieu affects cellular or exosome-associated human antigen R and what implications this has for cardiac inflammation and fibrosis.
Does targeting exosome-associated human antigen R (HuR) via knockdown attenuate cardiac fibrosis and inflammation in diabetic models?
Population
Human failing hearts, diabetic mice, db/db mice, and cultured macrophages and fibroblasts
Comparison
Reconstitution with BMMØ-derived HuR-deficient exosomes vs control-exosome administration
Design
Preclinical in vitro and in vivo study
Authors
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Hypothesis-generating in diabetic mice; leaves open HuR exosome targeting for human cardiac fibrosis.
Does targeting exosome-associated human antigen R (HuR) via knockdown attenuate cardiac fibrosis and inflammation in diabetic models?
Targeting exosome-associated HuR in macrophages attenuates pathological cardiac fibrosis and preserves left ventricular function in diabetic models, highlighting a potential novel therapeutic target.
Govindappa et al. (2019) studied this question.
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