What question did this study set out to answer?

To examine whether trimetazidine protects against pressure overload-induced heart failure by improving cardiac energy metabolism and to identify the role of AMPK signaling.

September 15, 2021Frontiers in PharmacologyOpen Access

Trimetazidine Attenuates Heart Failure by Improving Myocardial Metabolism via AMPK

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Why the study?

Energetic deficiency of cardiomyocytes causes heart failure, and it was hypothesized that trimetazidine protects cardiomyocytes from pressure overload-induced heart failure by improving myocardial metabolism.

Does trimetazidine improve left ventricular function and myocardial metabolism in pressure overload-induced heart failure models?

Population

C57BL/6 mice subjected to TAC and neonatal rat cardiomyocytes subjected to mechanical stretch

Comparison

Trimetazidine vs untreated controls with or without compound C

Design

Preclinical animal and in vitro laboratory study

Follow-up

4 weeks

Authors

HSHongyang ShuGangneung–Wonju National University WHWeijian HangFudan University YPYizhong PengUnion Hospital

Discussion

Member takes

Implication

Supports trimetazidine via AMPK in TAC models; leaves open clinical translation in human pressure-overload HF.

Key Points

To examine whether trimetazidine protects against pressure overload-induced heart failure by improving cardiac energy metabolism and to identify the role of AMPK signaling.
Subjected C57BL/6 mice to transverse aortic constriction (TAC) for four weeks to induce heart failure, treating cohorts with trimetazidine and the AMPK inhibitor compound C.
Evaluated left ventricular chamber dimensions, ejection fraction, mitochondrial morphology, cardiac glucose uptake, and GLUT4 translocation in vivo.
Assessed mechanical stretch-induced hypertrophy, mitochondrial dysfunction, and glucose uptake in neonatal rat cardiomyocytes in vitro with or without compound C.
Trimetazidine significantly prevented left ventricular dilation, preserved ejection fraction, and restored mitochondrial structure and dynamic proteins following TAC.
Treatment improved myocardial glucose uptake, preserved insulin signaling, and promoted GLUT4 membrane translocation, but these benefits were abolished by compound C.
In vitro, trimetazidine significantly reduced cardiomyocyte enlargement and mitochondrial deformation while increasing glucose uptake in an AMPK-dependent manner.

Structured PICO

Does trimetazidine improve left ventricular function and myocardial metabolism in pressure overload-induced heart failure models?

Population

C57BL/6 mice subjected to transverse aortic constriction (TAC) and neonatal rat cardiomyocytes subjected to mechanical stretch

Intervention

Trimetazidine

Comparator

Untreated TAC mice and untreated mechanically stretched cardiomyocytes

Outcome

Left ventricular chamber dimension and left ventricular ejection fraction evaluated by echocardiographysurrogate

Trimetazidine protects against pressure overload-induced heart failure by improving myocardial mitochondrial function and glucose uptake via AMPK activation in preclinical models.

Cite This Study

Shu et al. (2021) studied this question.

synapsesocial.com/papers/6a829d91d88fdfcf4fa0c192 https://doi.org/10.3389/fphar.2021.707399

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Trimetazidine Attenuates Heart Failure by Improving Myocardial Metabolism via AMPK

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Trimetazidine Attenuates Heart Failure by Improving Myocardial Metabolism via AMPK

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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