Key result
Hyperglycemic memory in diabetic cardiomyopathy stems from advanced glycation, microRNAs, oxidative stress, and epigenetic modifications.
Why the study?
Intensive glycemic control fails to reduce heart failure-associated hospitalization and mortality in diabetes, indicating persistent cardiovascular hyperglycemic stress known as hyperglycemic memory.
This review outlines the epigenetic, molecular, and metabolic mechanisms of hyperglycemic memory that perpetuate diabetic cardiomyopathy and cardiovascular risk despite subsequent intensive glycemic control.
May inform targeted therapies for persistent diabetic cardiomyopathy risk; leaves open validation in prospective interventional trials.
Cardiovascular diseases account for approximately 80% of deaths among individuals with diabetes mellitus, with diabetic cardiomyopathy as the major diabetic cardiovascular complication. Hyperglycemia is a symptom that abnormally activates multiple downstream pathways and contributes to cardiac hypertrophy, fibrosis, apoptosis, and other pathophysiological changes. Although glycemic control has long been at the center of diabetes therapy, multicenter randomized clinical studies have revealed that intensive glycemic control fails to reduce heart failure-associated hospitalization and mortality in patients with diabetes. This finding indicates that hyperglycemic stress persists in the cardiovascular system of patients with diabetes even if blood glucose level is tightly controlled to the normal level. This process is now referred to as hyperglycemic memory (HGM) phenomenon. We briefly reviewed herein the current advances that have been achieved in research on the underlying mechanisms of HGM in diabetic cardiomyopathy.
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Zhan et al. (2021) conducted a review in Diabetic cardiomyopathy. Hyperglycemic memory in diabetic cardiomyopathy is driven by a complex network of mechanisms including advanced glycation end products, microRNAs, mitochondrial oxidative stress, and epigenetic modifications.
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