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Tania Medali Biological Adaptation and Ageing (B2A), CNRS UMR-8256/INSERM ERL U-1164, Biological Institute Paris-Seine, Sorbonne University, Paris, France

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Dominique Couchie Biological Adaptation and Ageing (B2A), CNRS UMR-8256/INSERM ERL U-1164, Biological Institute Paris-Seine, Sorbonne University, Paris, France

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Nathalie Mougenot Plateforme PECMV, UMS28 INSERM, Faculté de Médecine, Sorbonne University, Paris, France

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Maria Mihoc Plateforme PECMV, UMS28 INSERM, Faculté de Médecine, Sorbonne University, Paris, France

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Olaf Bergmann Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden CRTD, TU Dresden, Dresden, Germany

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Wouter Derks Department of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden CRTD, TU Dresden, Dresden, Germany

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Celio X Santos BHF Centre of Excellence King's College London, The James Black Centre, London, UK

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Bertrand Friguet Biological Adaptation and Ageing (B2A), CNRS UMR-8256/INSERM ERL U-1164, Biological Institute Paris-Seine, Sorbonne University, Paris, France

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Mustapha Rouis Biological Adaptation and Ageing (B2A), CNRS UMR-8256/INSERM ERL U-1164, Biological Institute Paris-Seine, Sorbonne University, Paris, France

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Graphical abstract

Experimental Myocardial infarction (MI) using ligation procedure induces cardiac dysfunction, high level of ROS, inflammation, apoptosis, fibrosis and cardiomyocyte (CM) loss. AAV overexpressing human Trx-2, specifically in CM mitochondria improves mouse cardiac function, reduces the size of cardiac infarct, increases the expression of cardiac anti-inflammatory markers, reduces apoptosis and oxidative stress. However, it does not increase CM proliferation.

Abstract

Introduction and objective

Myocardial infarction (MI), which in general results from complications of atherosclerosis, is characterized by high inflammation and cardiomyocytes (CMs) apoptosis and by major loss of CMs. Regeneration of these lost CMs represents a major challenge for MI therapy. The increase of mitochondrial reactive oxygen species (ROS) is involved in cell cycle arrest which can be restarted by hypoxia or in the presence of ROS scavengers. Among ROS scavengers, mitochondrial thioredoxin 2 (Trx-2), an important antioxidant protein, could play a role in the CMs renewal.

Method

In this study, we investigated the effect of Trx-2 on mouse heart after an experimental MI.

Results

Trx-2 improves mouse cardiac function, reduces cardiac infarction size and increases the expression of cardiac anti-inflammatory markers. In addition, it reduces apoptosis and oxidative stress in heart tissue of mice after MI but it does not increase CM proliferation in cell culture or in heart tissue.

Conclusion

Mitochondrial Trx-2 effectively protects against heart infarction, likely via the reduction of oxidative stress, inflammation and apoptosis but not through CM renewal.

Significance statement

The current study unveils the complexities of MI and highlights mitochondrial Trx-2 role. Post-MI, marked by inflammation, CM apoptosis and significant CM loss. Trx-2 emerges as a vital protector. Its intervention improves mouse cardiac function, reduces infarction size and fosters an anti-inflammatory environment. By uncovering these mechanisms, the study suggests potential therapeutic strategies for oxidative stress, inflammation and apoptosis in MI, positioning Trx-2 as a promising candidate for future cardiac interventions.

Open access