Valeria Garrido, Evelyn Mendoza-Torres, Jaime A. Riquelme, Ariel Díaz, Marcela Pizarro, Mario Bustamante, Myra N. Chavez, María Paz Ocaranza, Rosemarie Mellado, Ramon Corbalan, Miguel L. Allende and Sergio Lavandero* Pages 2592 - 2615 ( 24 )
Cardiovascular disease is the leading cause of death worldwide. The heart is susceptible to pathologies that impact the myocardium directly, such as myocardial infarction and consequent heart failure, as well as conditions with indirect cardiac effects, such as cancer treatment-related cardiotoxicity. As the contractile cells of the heart, cardiomyocytes are essential for normal cardiac function. Various stress stimuli may result in transient damage or cell death in cardiomyocytes through apoptosis, necrosis or maladaptive autophagy. Moreover, cardiomyocytes are unable to regenerate; thus, lost cells are replaced with fibrotic tissue, with a potentially severe impact on myocardial function. Several therapeutic agents and strategies to reduce cardiomyocyte damage are currently available. This manuscript reviews the state of the art regarding novel cardioprotective endogenous peptides, such as neuregulin-1, angiotensin-(1-9), growth/differentiation factor-11, growth/differentiation factor- 15 and insulin-like growth factor-1. We discuss their protective effects and therapeutic potential in cardiovascular diseases and the current challenges to harnessing their full cardioprotective power. We also explore targeting of exosomes as a cardioprotective approach along with the therapeutic potential of cardiac regeneration strategies. Further advances associated with these molecules and cardioprotective approaches may provide more effective therapies to attenuate or prevent cardiomyocyte death, thereby preserving the myocardium.
Cell death, cardio-oncology, neuregulin-1, angiotensin-(1-9), growth differentiation factor, insulin-like growth factor-1, exosomes, cardiac regeneration, cardiovascular diseases.
Advanced Center for Chronic Diseases (ACCDiS) & Center for Molecular Studies of the Cell (CEMC), Faculty of Chemical and Pharmaceutical Sciences & Faculty of Medicine, University of Chile, Santiago, Faculty of Health Sciences, Universidad Libre, Barranquilla, Advanced Center for Chronic Diseases (ACCDiS) & Center for Molecular Studies of the Cell (CEMC), Faculty of Chemical and Pharmaceutical Sciences & Faculty of Medicine, University of Chile, Santiago, Advanced Center for Chronic Diseases (ACCDiS) & Center for Molecular Studies of the Cell (CEMC), Faculty of Chemical and Pharmaceutical Sciences & Faculty of Medicine, University of Chile, Santiago, Advanced Center for Chronic Diseases (ACCDiS) & Center for Molecular Studies of the Cell (CEMC), Faculty of Chemical and Pharmaceutical Sciences & Faculty of Medicine, University of Chile, Santiago, Advanced Center for Chronic Diseases (ACCDiS), Cardiovascular Division, Faculty of Medicine, Pontifical Catholic University of Chile, Santiago, Advanced Center for Chronic Diseases (ACCDiS) & Center for Molecular Studies of the Cell (CEMC), Faculty of Chemical and Pharmaceutical Sciences & Faculty of Medicine, University of Chile, Santiago, Advanced Center for Chronic Diseases (ACCDiS), Cardiovascular Division, Faculty of Medicine, Pontifical Catholic University of Chile, Santiago, Faculty of Chemistry, Pontifical Catholic University of Chile, Santiago, Advanced Center for Chronic Diseases (ACCDiS), Cardiovascular Division, Faculty of Medicine, Pontifical Catholic University of Chile, Santiago, Center for Genome Regulation, Department of Biology, Faculty of Sciences, University of Chile, Santiago, Advanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Olivos 1007, Santiago 8380492