Cardiovascular diseases as myocardial infarction (MI) represent a major cause for morbidity and mortality worldwide. Even though, patients who survive MI are susceptible to high risk of heart failure. This is mainly attributed to the major loss of cardiomyocytes and limited regenerative potential of myocardium. Despite the availability of various cardiovascular drugs, they fail to address the main cause of MI. The optimum therapeutic goal should therefore focus on enhancing cardiac regeneration through cellular and cell-free therapeutic approaches. This review focused on different mechanisms of cardiac regeneration that can be achieved via non-cellular therapeutic modalities. Passive and active targeting of the infarcted myocardium using various nanoparticles that can be loaded with growth factors, drugs or affordable natural products can reduce negative ventricular remodeling, infarct size and the apoptotic rate of cardiomyocytes. In addition, injectable biomaterials-based nanocomposite can be used as a scaffold to support infarcted heart and recruit cells. Innovative affordable and less invasive cell-free approaches can be implemented to enhance cardiac regeneration post MI.
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http://dx.doi.org/10.1007/s13346-024-01763-y | DOI Listing |
Curr Cardiol Rep
January 2025
Department of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY, 10029, USA.
Purpose Of The Review: This review aims to discuss the process of cardiomyocyte maturation, with a focus on the underlying molecular mechanisms required to form a fully functional heart. We examine both long-standing concepts associated with cardiac maturation and recent developments, and the overall complexity of molecularly integrating all the processes that lead to a mature heart.
Recent Findings: Cardiac maturation, defined here as the sequential changes that occurring before the heart reaches full maturity, has been a subject of investigation for decades.
Heliyon
January 2025
Department of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
The extracellular matrix (ECM) is a complex and dynamic three-dimensional network that functions as an architectural scaffold to maintain cardiac homeostasis. Important biochemical and mechanical signals associated with cell‒cell communication are provided via the reciprocal interaction between cells and the ECM. By converting mechanical cues into biochemical signals, the ECM regulates many cell processes, including migration, adhesion, growth, differentiation, proliferation, and apoptosis.
View Article and Find Full Text PDFFront Cell Dev Biol
January 2025
Department of Human Genetics, Leiden University Medical Center (LUMC), Leiden, Netherlands.
Muscle repair and regeneration are complex processes. In Duchenne muscular dystrophy (DMD), these processes are disrupted by the loss of functional dystrophin, a key part of the transmembrane dystrophin-associated glycoprotein complex that stabilizes myofibers, indirectly leading to progressive muscle wasting, subsequent loss of ambulation, respiratory and cardiac insufficiency, and premature death. As part of the DMD pathology, histone deacetylase (HDAC) activity is constitutively increased, leading to epigenetic changes and inhibition of muscle regeneration factors, chronic inflammation, fibrosis, and adipogenesis.
View Article and Find Full Text PDFApoptosis
January 2025
National Traditional Chinese Medicine Clinical Research Base, Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, 646000, Sichuan, People's Republic of China.
Cardiovascular disease (CVD) is a leading cause of human mortality worldwide, with patients often at high risk of heart failure (HF) in myocardial infarction (MI), a common form of CVD that results in cardiomyocyte death and myocardial necrosis due to inadequate myocardial perfusion. As terminally differentiated cells, cardiomyocytes possess a severely limited capacity for regeneration, and an excess of dead cardiomyocytes will further stress surviving cells, potentially exacerbating to more extensive heart disease. The article focuses on the relationship between programmed cell death (PCD) of cardiomyocytes, including different forms of apoptosis, necrosis, and autophagy, and MI, as well as the potential application of these mechanisms in the treatment of MI.
View Article and Find Full Text PDFDrug Deliv Transl Res
January 2025
Department of Pharmaceutics, Faculty of Pharmacy, Alexandria University, 1 Khartoum Square, Azarita, P.O. Box 21521, Alexandria, Egypt.
Cardiovascular diseases as myocardial infarction (MI) represent a major cause for morbidity and mortality worldwide. Even though, patients who survive MI are susceptible to high risk of heart failure. This is mainly attributed to the major loss of cardiomyocytes and limited regenerative potential of myocardium.
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