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Silencing Survivin: a Key Therapeutic Strategy for Cardiac Hypertrophy


Cardiac hypertrophy, in its aspects of localized thickening of the interventricular septum and concentric increase of the left ventricle, constitutes a risk factor of heart failure. Myocardial hypertrophy, in the presence of different degree of myocardial fibrosis, is paralleled by significant molecular, cellular, and histological changes inducing alteration of cardiac extracellular matrix composition as well as sarcomeres and cytoskeleton remodeling. Previous studies indicate osteopontin (OPN) and more recently survivin (SURV) overexpression as the hallmarks of heart failure although SURV function in the heart is not completely clarified. In this study, we investigated the involvement of SURV in intracellular signaling of hypertrophic cardiomyocytes and the impact of its transcriptional silencing, laying the foundation for novel target gene therapy in cardiac hypertrophy. Oligonucleotide-based molecules, like theranostic optical nanosensors (molecular beacons) and siRNAs, targeting SURV and OPN mRNAs, were developed. Their diagnostic and therapeutic potential was evaluated in vitro in hypertrophic FGF23-induced human cardiomyocytes and in vivo in transverse aortic constriction hypertrophic mouse model. Engineered erythrocyte was used as shuttle to selectively target and transfer siRNA molecules into unhealthy cardiac cells in vivo. The results highlight how the SURV knockdown could negatively influence the expression of genes involved in myocardial fibrosis in vitro and restores structural, functional, and morphometric features in vivo. Together, these data suggested that SURV is a key factor in inducing cardiomyocytes hypertrophy, and its shutdown is crucial in slowing disease progression as well as reversing cardiac hypertrophy. In the perspective, targeted delivery of siRNAs through engineered erythrocytes can represent a promising therapeutic strategy to treat cardiac hypertrophy.

Graphical abstract

Theranostic SURV molecular beacon (MB-SURV), transfected into FGF23-induced hypertrophic human cardiomyocytes, significantly dampened SURV overexpression. SURV down–regulation determines the tuning down of MMP9, TIMP1 and TIMP4 extracellular matrix remodeling factors while induces the overexpression of the cardioprotective MCAD factor, which counterbalance the absence of pro-survival and anti-apoptotic SURV activity to protect cardiomyocytes from death. In transverse aortic constriction (TAC) mouse model, the SURV silencing restores the LV mass levels to values not different from the sham group and counteracts the progressive decline of EF, maintaining its values always higher with respect to TAC group. These data demonstrate the central role of SURV in the cardiac reverse remodeling and its therapeutic potential to reverse cardiac hypertrophy.

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Atrial natriuretic peptide


Blackberry Quencher 650


Beta- myosin heavy chain


Brain natriuretic peptide


Confocal laser scanning microscopy


Cross-sectional area


Ejection fraction


Early growth response 1


Erythro-Magneto-Ha virosome


Extracellular signal-regulated kinases


Fibroblast growth factor 23


Filamentous hemagglutinin


Fractional shortening


Glyceraldehyde-3-phosphate dehydrogenase


Human cardiomyocyte


Heart failure


Horseradish peroxidase


Heart weight




Interventricular septum thickness, diastolic


Left carotid


Left ventricle


Left ventricular assist device


Left ventricle posterior wall thickness, diastolic


Molecular beacon


Medium-chain acyl-CoA dehydrogenase


Matrix metalloproteinase


Nitric oxide


NADPH oxidase 4




Pixel fluorescence signal


Right carotid




Super-paramagnetic iron oxide nanoparticles




Transverse aortic constriction


Tissue inhibitor of metalloproteinase


Tibia length


Ultra high-frequency ultrasound


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The authors thank Dr. Silvia Burchielli for supporting animal protocol preparation and internal ethical committee.


This work was supported by National Flagship project NANOMAX-ENCODER of the Italian Ministry of Education, University and Research.

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Correspondence to Maria Giovanna Trivella or Caterina Cinti.

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Kusmic, C., Vizzoca, A., Taranta, M. et al. Silencing Survivin: a Key Therapeutic Strategy for Cardiac Hypertrophy. J. of Cardiovasc. Trans. Res. (2021).

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  • Cardiac hypertrophy
  • Target therapy
  • Surviving
  • Erythrocyte-based drug delivery system