Abstract
Cardiovascular diseases (CVD) are the leading cause of morbidity and mortality worldwide. Conventional therapies involving surgery or pharmacological strategies have shown limited therapeutic effects due to a lack of cardiac tissue repair. Gene therapy has opened an avenue for the treatment of cardiac diseases through manipulating the underlying gene mechanics. Several gene therapies for cardiac diseases have been assessed in clinical trials, while the clinical translation greatly depends on the delivery technologies. Non-viral vectors are attracting much attention due to their safety and facile production compared to viral vectors. In this review, we discuss the recent progress of non-viral gene therapies for the treatment of cardiovascular diseases, with a particular focus on myocardial infarction (MI). Through a summary of delivery strategies with which to target cardiac tissue and different cardiac cells for MI treatment, this review aims to inspire new insights into the design/exploitation of non-viral delivery systems for gene cargos to promote cardiac repair/regeneration.
Highlights
Cardiovascular diseases (CVD) are the leading cause of death worldwide
Blockades in blood vessels immediately interrupt the supply of oxygen and nutrients, and if the blockades cannot be removed within 15 min, the cells in the infarct zone begin to die and release chemotactic factors that initiate acute and chronic inflammatory processes, eventually causing ventricle dilation and heart failure [4]
All the results show that, compared to unmodified vehicles, Cell penetrating peptides (CPPs) did enhance the internalization of delivery systems in CMs, while simple cationic particles, such as those made from polyamidoamine (PAMAM) and PEI, failed to achieve efficient delivery [77,78]
Summary
Cardiovascular diseases (CVD) are the leading cause of death worldwide. Among the types of CVD, ischemic heart diseases (IHD) ranked first for disease burden in 2015 [3]. Is a form of IHD and is usually caused by the occlusion of coronary arteries due to floating atherosclerotic plaques. Blockades in blood vessels immediately interrupt the supply of oxygen and nutrients, and if the blockades cannot be removed within 15 min, the cells in the infarct zone begin to die and release chemotactic factors that initiate acute and chronic inflammatory processes, eventually causing ventricle dilation and heart failure [4]. The therapeutic outcomes of current surgical interventions or pharmacological treatments are limited due to the failure to repair infarcted tissue [5], implying an urgent need for new, alternative strategies
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