Key result
Ciglitazone or tempol mitigates homocysteine-exacerbated diabetic cardiomyopathy by restoring endothelial-myocyte coupling.
Why the study?
The synergistic contribution of hyperhomocysteinemia and hyperglycemia to diabetic cardiomyopathy and the role of PPAR gamma attenuation were unclear.
Does treatment with ciglitazone or tempol improve cardiac remodeling and diastolic dysfunction in a mouse model of diabetes and hyperhomocysteinemia?
Population
Diabetic Akita (Ins2+/-), hyperhomocysteinemic CBS+/- and hybrid mice
Comparison
Ciglitazone and tempol treatments versus vehicle
Design
Preclinical study with cardiac functional and molecular assessments
Follow-up
4 weeks
Authors
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Hypothesis-generating for diabetic cardiomyopathy mechanisms; human studies required before any clinical translation.
Does treatment with ciglitazone or tempol improve cardiac remodeling and diastolic dysfunction in a mouse model of diabetes and hyperhomocysteinemia?
In a mouse model, hyperhomocysteinemia and hyperglycemia synergistically exacerbate diabetic cardiomyopathy, which can be mitigated by PPAR gamma agonists or antioxidants.
Mishra et al. (2010) studied Diabetic cardiomyopathy. Ciglitazone and Tempol vs. Vehicle (normal drinking water) was evaluated on Cardiac remodeling and diastolic dysfunction. Endogenous homocysteine exacerbates diabetic cardiomyopathy by attenuating PPAR gamma and inducing endothelial-myocyte uncoupling, which is mitigated by treatment with ciglitazone or tempol.
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