Why the study?
Melatonin attenuates diabetic cardiomyopathy, but the underlying mechanism and the role of VEGF-B remain unclear.
Does melatonin improve cardiac dysfunction in type 1 diabetes mellitus induced cardiomyopathy mice?
Population
T1DM-induced cardiomyopathy mice and high glucose-treated neonatal rat ventricular myocytes
Comparison
Melatonin vs controls with VEGF-B, PERK, or autophagy modulation
Design
Preclinical animal and cellular experimental study
Key result
Melatonin significantly alleviated cardiac dysfunction and improved autophagy of cardiomyocytes in type 1 diabetes mellitus-induced cardiomyopathy mice via the VEGF-B/GRP78/PERK signaling pathway.
Authors
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Does not support clinical use in diabetic cardiomyopathy; leaves open human translation of this pathway.
Does melatonin improve cardiac dysfunction in type 1 diabetes mellitus induced cardiomyopathy mice?
p-value: p=<0.05
Melatonin attenuates diabetic cardiomyopathy by increasing cardiomyocyte autophagy via the VEGF-B/GRP78/PERK signaling pathway, suggesting a potential therapeutic target for diabetic cardiomyopathy.
Zhang et al. (2024) studied Diabetic cardiomyopathy (n=42). Melatonin vs. Saline was evaluated on Cardiac function (ejection fraction and fractional shortening) and cardiomyocyte autophagy (p=<0.05). Melatonin significantly alleviated cardiac dysfunction and improved autophagy of cardiomyocytes in type 1 diabetes mellitus-induced cardiomyopathy mice via the VEGF-B/GRP78/PERK signaling pathway.
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