March 16, 2022Frontiers in Cardiovascular MedicineOpen Access

Hypoglycemia challenge aggravated cardiac diastolic dysfunction and induced Cx43 translocation to mitochondria via MEK/ERK/Src and PI3K/Akt/Src pathways; mtCx43 overexpression recapitulated these defects in vivo.

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Why the study?

Hypoglycemia increases sudden death risk in diabetes mellitus, but the molecular mechanisms by which it aggravates diabetic cardiomyopathy progression remain to be elucidated.

Does hypoglycemia challenge exacerbate cardiac dysfunction and aberrant electrophysiology in diabetic cardiomyopathy models?

Population

Streptozotocin-induced DCM mice, neonatal mouse ventricular myocytes, and cardiomyocytes from patients with DM

Comparison

Hypoglycemia challenge and mtCx43 overexpression vs controls

Design

Preclinical animal and cellular mechanistic study

Authors

XWXing Wei ACAndrew Chia Hao Chang HCHaishuang Chang

Discussion

Member takes

Overview

Should not yet change practice; leaves open mitochondrial connexin 43 as a therapeutic target in hypoglycemia-aggravated DCM.

Structured PICO

Does hypoglycemia challenge exacerbate cardiac dysfunction and aberrant electrophysiology in diabetic cardiomyopathy models?

Population

Streptozotocin (STZ)-induced diabetic cardiomyopathy (DCM) murine model (8-week-old C57BL/6N mice), neonatal mouse ventricular myocytes (NMVMs), and human cardiac tissue from patients with diabetes mellitus.

Intervention

Hypoglycemia challenge (insulin 100 IU intraperitoneal injection in vivo; glucose fluctuation in vitro) and overexpression of mitochondrial targeting Cx43 (mtCx43) using adeno-associated virus serotype 2 (AAV2)/9.

Comparator

Normoglycemia controls, sodium citrate-injected control mice, and wild-type Cx43 or GFP overexpression controls.

Outcome

Cardiac diastolic function (E/A ratio, E/E' ratio), electrophysiology (ECG parameters including QTc, QT, QRS, JT intervals), and Cx43 accumulation at the mitochondrial inner membrane.surrogate

Hypoglycemia exacerbates diabetic cardiomyopathy by promoting mitochondrial accumulation of Connexin 43, identifying mtCx43 as a potential therapeutic target to prevent hypoglycemia-induced cardiac dysfunction.

Cite This Study

Wei et al. (2022) studied this question.

synapsesocial.com/papers/6a7f5e77ae0800d85efbefa4 https://doi.org/10.3389/fcvm.2022.800185

View Full Paper

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March 16, 2022Frontiers in Cardiovascular MedicineOpen Access

Hypoglycemia challenge aggravated cardiac diastolic dysfunction and induced Cx43 translocation to mitochondria via MEK/ERK/Src and PI3K/Akt/Src pathways; mtCx43 overexpression recapitulated these defects in vivo.

View Full Paper

Ask AI

Bookmark

Why the study?

Hypoglycemia increases sudden death risk in diabetes mellitus, but the molecular mechanisms by which it aggravates diabetic cardiomyopathy progression remain to be elucidated.

Does hypoglycemia challenge exacerbate cardiac dysfunction and aberrant electrophysiology in diabetic cardiomyopathy models?

Population

Streptozotocin-induced DCM mice, neonatal mouse ventricular myocytes, and cardiomyocytes from patients with DM

Comparison

Hypoglycemia challenge and mtCx43 overexpression vs controls

Design

Preclinical animal and cellular mechanistic study

Authors

XWXing Wei ACAndrew Chia Hao Chang HCHaishuang Chang

Discussion

Member takes

Overview

Should not yet change practice; leaves open mitochondrial connexin 43 as a therapeutic target in hypoglycemia-aggravated DCM.

Structured PICO

Does hypoglycemia challenge exacerbate cardiac dysfunction and aberrant electrophysiology in diabetic cardiomyopathy models?

Population

Intervention

Comparator

Normoglycemia controls, sodium citrate-injected control mice, and wild-type Cx43 or GFP overexpression controls.

Outcome

Cardiac diastolic function (E/A ratio, E/E' ratio), electrophysiology (ECG parameters including QTc, QT, QRS, JT intervals), and Cx43 accumulation at the mitochondrial inner membrane.surrogate

Cite This Study

Wei et al. (2022) studied this question.

synapsesocial.com/papers/6a7f5e77ae0800d85efbefa4 https://doi.org/10.3389/fcvm.2022.800185

Also Consider

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