Key result
Accumulation of advanced glycation end products in diabetic patients was associated with post-myocardial infarction ventricular arrhythmias via the RAGE-dependent ER stress PERK pathway.
Why the study?
Patients after myocardial infarction are more vulnerable to ventricular arrhythmias when complicated with diabetes, but the underlying mechanism remains to be interpreted.
What is the mechanism underlying the increased vulnerability to post-myocardial infarction ventricular arrhythmias in patients with diabetes?
Cohort
What is the mechanism underlying the increased vulnerability to post-myocardial infarction ventricular arrhythmias in patients with diabetes?
The study identifies the RAGE-dependent ER stress PERK pathway as a key mechanism for the increased vulnerability to post-MI ventricular arrhythmias in diabetic patients.
May support RAGE-PERK targeting to mitigate post-MI VAs in diabetes; hypothesis-generating and requires randomized validation before practice change.
In this study, we proposed a possible mechanism interpreting the clinical scenario that after myocardial infarction (MI) patients were more vulnerable to ventricular arrhythmias (VAs) when complicated with diabetes. A cohort study revealed that advanced glycation end products (AGEs) accumulated in patients with diabetes and closely associated post-MI VAs. In vivo and in vitro studies indicated that receptor for AGEs (RAGE)-dependent endoplasmic reticulum (ER) stress protein kinase RNA-like ER kinase (PERK) pathway triggered VAs, via ER calcium releasing, through calcineurin/RyR2 mechanism.
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Liu et al. (2021) conducted a cohort in Myocardial infarction complicated with diabetes. Advanced glycation end products (AGEs) was evaluated on Post-myocardial infarction ventricular arrhythmias. Accumulation of advanced glycation end products in diabetic patients was associated with post-myocardial infarction ventricular arrhythmias via the RAGE-dependent ER stress PERK pathway.
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