Why the study?
It was unknown whether secreted frizzled-related protein 2 (SFRP2) regulates oxidative stress and apoptosis through mitochondrial function in diabetic cardiomyopathy.
Does SFRP2 overexpression improve mitochondrial function, oxidative stress, and apoptosis in models of diabetic cardiomyopathy?
Population
H9C2 cardiomyocytes and an SD rat model of T2DM
Comparison
SFRP2 overexpression or knockdown vs controls under glucolipotoxic or diabetic conditions
Design
In vitro and in vivo preclinical laboratory study
Key result
SFRP2 overexpression exerted cardioprotective effects in diabetic cardiomyopathy models by salvaging mitochondrial function in an AMPK-PGC1-α-dependent manner, reducing oxidative stress and apoptosis.
Authors
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Hypothesis-generating for SFRP2 in diabetic cardiomyopathy; human trials needed before clinical translation.
Does SFRP2 overexpression improve mitochondrial function, oxidative stress, and apoptosis in models of diabetic cardiomyopathy?
SFRP2 exerts cardioprotective effects in diabetic cardiomyopathy models by salvaging mitochondrial function via the AMPK-PGC1-α pathway.
Ma et al. (2021) studied Diabetic cardiomyopathy. SFRP2 overexpression vs. Control/normal conditions was evaluated on Mitochondrial dynamics, oxidative stress, and apoptosis. SFRP2 overexpression exerted cardioprotective effects in diabetic cardiomyopathy models by salvaging mitochondrial function in an AMPK-PGC1-α-dependent manner, reducing oxidative stress and apoptosis.
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