Why the study?
Patients with T2DM face an increased risk of MI, but the molecular mechanisms underlying MI injury in T2DM remain elusive.
Does FSTL1 treatment improve cardiac function and reduce myocardial fibrosis in T2DM mice following MI?
Does FSTL1 treatment improve cardiac function and reduce myocardial fibrosis in T2DM mice following MI?
FSTL1 gene therapy ameliorates post-MI cardiac dysfunction and fibrosis in diabetic mice via the USP10/Notch1 signaling pathway.
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May identify USP10/FSTL1 as targets in diabetic MI; leaves open clinical translation pending prospective validation.
Lu et al. (2021) studied this question.
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